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In the diagnosis of a given disease it is essential that the physician rest 
his opinion not upon one or two symptoms, but upon a series of symptoms 
which when properly put together give him a complete, or nearly a complete, 
picture of the malady. It is as futile for a physician to attempt to base a 
diagnosis upon a single symptom as for an architect to attempt to determine 
the appearance of a house by seeing one of the stones which has been removed 
from its walls. 



DIAGNOSIS 



IN THE 



OFFICE AND AT THE BEDSIDE 

THE USE OF SYMPTOMS AND PHYSICAL 
SIGNS IN THE DIAGNOSIS OF DISEASE 



BY 

HOBART AMORY HARE, M.D., B.Sc. 

PROFESSOR OF THERAPEUTICS, MATERIA MEDICA, AND DIAGNOSIS IN THE JEFFERSON MEDICAL 

COLLEGE OF PHILADELPHIA: PHYSICIAN TO THE JEFFERSON MEDICAL COLLEGE HOSPITAL; 

ONE TIME CLINICAL PROFESSOR OF DISEASES OF CHILDREN IN THE UNIVERSITY OF 

PENNSYLVANIA; AUTHOR OF A TEXT-BOOK OF PRACTICAL THERAPEUTICS 

AND A TEXT-BOOK OF THE PRACTICE OF MEDICINE 



SEVENTH EDITION, THOROUGHLY REVISED 



ILLUSTRATED WITH 164 ENGRAVINGS AND 10 PLATES 




LEA & FEBIGER 

PHILADELPHIA AND NEW YORK 
1914 






Entered according to the Act of Congress, in the year 19 14, by 

LEA & FEBIGER, 
in the office of the Librarian of Congress. All rights reserved. 



FEB -5 1914 

©CI.A362465 









THIS BOOK 



is 



DEDICATED TO MY FRIEND AND COLLEAGUE 

J. CHALMERS Da COSTA, M.D., 

PROFESSOR OF THE PRINCIPLES OF SURGERY AND CLINICAL SURGERY 
IN THE JEFFERSON MEDICAL COLLEGE OF PHILADELPHIA. 



PREFACE TO SEVENTH EDITION. 



This volume is essentially devoted to a plan whereby a 
recognition of symptoms will lead the physician to a diagnosis. 
To accomplish this the symptoms used in diagnosis are dis- 
cussed first, and their application to determine the character 
of the disease follows. Thus, instead of describing locomotor 
ataxia or myelitis, there will be found in the chapter on the 
Feet and Legs a discussion of the various forms of loss of 
power in the legs, so that the physician who is consulted by a 
paraplegic patient will be able readily to reach a diagnosis. In 
the chapter on Cough and Expectoration it is pointed out that 
hemoptysis may be due not only to pulmonary tuberculosis, but 
also to cardiac valvular disease, to pulmonary infarction, thoracic 
aneurysm, bronchiectasis and purpura, and these facts lead to 
differentiation. So, too, in the chapter on Vomiting, its signifi- 
cance, both local and remote, is discussed. In other words, this 
book is written upon the plan which is actually followed in practice, 
namely, the upbuilding of a diagnosis by grouping the symptoms. 
Under the older methods the reverse of this plan was followed, 
whereby the physician was compelled to make a supposititious 
diagnosis and then to turn to his reference book to compare the 
symptoms of his patient with the text dealing with the supposed 
disease. If the description failed to coincide with the symptoms 
of his case he was forced to make another guess and read another 
article. 

Laboratory diagnosis is now so highly developed that it requires 
special volumes for its description. As there are several excellent 
books of this character, the author has omitted laboratory methods 
from his text in order that his intention of considering symptoms 
as they appear in the orifice and at the bedside may be the better 
carried out. 

H. A. H. 

N. W. COR. EIGHTEENTH AND SPRUCE STREETS, 
PHILADELPHIA, JANUARY, I9I4. 



CONTENTS. 



INTRODUCTION. 
GENERAL DIAGNOSTIC CONSIDERATIONS. 



CHAPTER I. 

THE FACE AND HEAD. 

The expression and color of the face — Facial deformity — Facial paralysis, 
unilateral and bilateral — Ptosis — Facial spasm — The shape of the 
head — The movements and position of the head and neck ... 25 

CHAPTER II. 

THE HANDS AND ARMS. 

The general appearance of the hands and arms — The shape of the hands 
in disease — Spasms of the fingers — Tremors of the hands — Paralysis 
of the hands and arms 49 

CHAPTER III. 

THE FEET AND LEGS. 

The general appearance of the feet and legs when clothed — The gait — 
Spastic paraplegia — Paraplegia without spastic contraction — Crural 
monoplegia — Deformities of the feet and legs — The joints — Altera- 
tions in the nutrition of the feet and legs aside from a change in the 
muscles 73 

CHAPTER IV. 

HEMIPLEGIA 112 

CHAPTER V. 
SPEECH. 

The changes in the speech and voice — Their significance — Aphasia — 

Apraxia — Alexia — Paraphasia 125 



X CONTENTS 

CHAPTER VI. 

THE SKIN. 

The color of the skin — Eruptions on the skin — Gangrene, ulcers, and 
sloughs — Scars, sweating, dryness, edema, hardness — Anesthesia and 
hemianesthesia — Paresthesia, hyperesthesia, itching 131 

CHAPTER VII. 

THE TONGUE, MOUTH, PHARYNX, AND (ESOPHAGUS. 

The general appearance of the tongue — Its coating — Its appearance 
in poisoning — Fissures and ulcers of the tongue — Eruptions on the 
tongue — Atrophy and hypertrophy of the tongue — Paralysis — Tremor 
and spasm of the tongue — Tonsillitis — Diphtheria — Pharyngitis — 
Disease of the oesophagus 191 

CHAPTER VIII. 

THE THORAX AND ITS VISCERA. 

The inspection of the normal and abnormal chest — Their topography — 
Alterations in the shape of the thorax — The rhythm of the respira- 
tions — The results of using inspection, palpation, percussion, and 
auscultation in health and disease — -The characteristic signs and 
symptoms of the various diseases of the thoracic organs . ... . 208 

CHAPTER IX. 

THE PULSE, BLOODVESSELS, AND BLOOD-PRESSURE. 

Feeling and counting the pulse — The condition of the bloodvessels on 
palpation — The quality, force, tension, and volume of the pulse in 
health and disease — Blood-pressure in health and disease . . . . 278 

CHAPTER X. 

THE ABDOMEN AND THE ABDOMINAL VISCERA. 

The surface of the abdomen — Changes in the appearance and shape of 
the abdominal wall — The signs and symptoms of disease of the 
abdominal organs 298 

CHAPTER XI. 

THE BOWELS AND FECES. 

Constipation and diarrhea — The cause of these two symptoms and their 
diagnosis — The diseases in which these symptoms occur — Choleraic 
diarrhea — Dysentery— The color of the feces— Intestinal parasites . 329 



CONTENTS XI 



CHAPTER XII 

THE URINARY BLADDER AND THE URINE. 

Disorders and diseases of the urinary bladder — Retention of urine — 
Incontinence of urine — The characteristics of normal and abnormal 
urine . • • 343 

CHAPTER XIII. 

THE EYE. 

The general diagnostic indications afforded by the eye — Diplopia and dis- 
order of the external ocular muscles— Strabismus and squint — Dis- 
order of the internal ocular muscles — The pupil — Hemianopsia — -The 
visual fields — Color vision — The optic nerve and its lesions — Retinitis 
— Amblyopia and blindness 359 

CHAPTER XIV. 

CHILLS, FEVERS, AND SUBNORMAL TEMPERATURES. 

Chills — The methods of taking the temperature — The significance of 

fever — The febrile movements of various diseases 390 

CHAPTER XV. 

HEADACHE AND VERTIGO. 

The causes of headache — Digestive headache — Headaches due to the 
eyes — Headaches due to cerebral growths and abscess — Headaches 
due to syphilis — Headaches complicating acute diseases . . . . 416 

CHAPTER XVI. 

COMA OR UNCONSCIOUSNESS 433 

CHAPTER XVII. 

CONVULSIONS OR GENERAL SPASMS. 

Definition of a convulsion — The convulsions of epilepsy in its various 
forms — Of infancy — Of hysteria — Tetanic convulsions — Tetany — 
Chorea 440 

CHAPTER XVIII. 

HICCOUGH, VOMITING, REGURGITATION, AND THE CHARACTER OF THE VOMIT. 

Due to uremia — Cerebral lesions — Intestinal obstruction — Peritonitis — 
Cholera— Gastric disease — Hepatic disease — Poisons — The appearance 
of vomit 455 



Xll CONTENTS 

CHAPTER XIX. 

COUGH AND EXPECTORATION. 

The varieties of and diagnostic significance of cough — The causes of 

cough — The sputum — Its pathological significance 471 

CHAPTER XX. 

PAIN. 

The kinds of pain — The significance of its locality — Colic . . . . 478 

CHAPTER XXL 

TENDON REFLEXES AND MUSCLE TONE. 

The knee-jerk and ankle clonus — The arm-jerk — The significance of 

decreased and increased reflexes 494 



DIAGNOSIS. 



INTRODUCTION. 

GENERAL DIAGNOSTIC CONSIDERATIONS. 

A clear understanding by the physician of the value of the 
symptoms of disease which he sees and of those described by the 
patient is of vital importance for the purpose of diagnosis and 
treatment, and one of the advantages of older physicians over their 
younger brethern is the ability which they have gained through 
long training to grasp the essential details of a case almost at their 
first glance at the patient. Much of this ability is unconsciously 
possessed because it is gained by a gradual process, yet it is none 
the less valuable, and its possession often impresses the patient 
with the insight which his physician has into his case. At first it is 
impossible for the novice to cast aside the minor symptoms, which 
the patient emphasizes as his major ones, and to perceive clearly 
that one or two facts that have been belittled in the narration of 
the story of the illness are in reality the stalk about which every- 
thing else in the case must be made to cluster. 

While the physician should train his eye to take note of all 
variations from the normal which are shown by the patient, he 
must be careful not to permit himself to depend for his diagnosis on 
these signs alone nor upon those described by the sick man. On 
the contrary, he should carefully train his senses of touch, hearing, 
sight, and discover the so-called physical signs which can be 
elicited only by auscultation, percussion, palpation, and mensu- 
ration. The objective symptoms seen by the physician, the sub- 
jective symptoms described by the patient, and the so-called 
physical signs elicited by the methods just named, are to be joined 
together in forming a diagnostic view of the case. Unless this 
combination is made, a faulty diagnosis will often be reached. In 
many instances chemical and microscopic examinations of the blood, 
the urine, the feces, and even of the tissues themselves, may be 
needful to determine in a given case what the ailment may be. 

Again, it is never to be forgotten that negative signs are as 
important as positive signs in many cases. The absence of a heart 



1 8 INTRODUCTION 

murmur in a case of failing circulation is not a sign that the heart 
valves are healthy, but that the heart is too feeble to make a 
murmur, and the absence of rales or clearly heard breath sounds 
in a lung may be due to engorgement without exudate instead 
of indicating that the lung is not diseased. 

The Art of Observing the Patient. — Let us suppose the patient 
before the physician is one who has been able to walk into the 
office or dispensary. The attentive physician can at once gather 
much information about the case from the clothing, the gait, the 
build, the voice, the expression, and the manner. The thin man, 
with a peaked face and provided with an unusually warm overcoat, 
and still further wrapped up with a muffler almost to his eyes, is 
in all probability a sufferer from some pulmonary or throat diffi- 
culty, while the heavily built, phlegmatic individual, with a large 
head and well-filled paunch, is much more apt to suffer from 
gastro-intestinal or biliary catarrhs. Such a person will probably 
be one who habitually wears his coat open on the coldest days. 
Again, chronic drunkards, or persons whose mental powers are 
failing, often are exceedingly careless about their clothing, button- 
ing the coat or the trousers with the wrong buttons, and keeping 
the garments dirty and spotted. Some cases of diabetes have first 
been discovered by the white spots on the trousers, as the result 
of the patient having allowed a few drops of urine to fall on the 
cloth, where they have dried. Old men who have incontinence 
of urine often wear trousers which are stained in front, and they 
often have an ammoniacal odor about them from this cause. 

The various forms of gait which indicate actual disease will 
be found discussed in the chapter on the Legs and Feet, but it 
may be mentioned in passing that, in addition to these changes, 
which are dependent upon actual disease of the legs or the nervous 
system supplying them, the bearing and stride of a patient will 
often give a clear idea of his general tone. The neurasthenic 
patient walks feebly or with a step that might be called ataxic, 
while the strong, hearty man of good physique strides along with 
a gait quite different from this, or from that of an individual who 
is delicate and feeble. 

Similarly, the patient's build betokens disease or health. The 
thin, tall, and hollow-chested person is recognized as a fair mark 
for the tubercle bacillus, and the heavy, closely knit, phlegmatic 
man as one who may suffer from hepatic or circulatory disorders. 
Again, the bearing of a person possessing a highly organized 
nervous system shows itself in the constant activity of his mind 
and body. No part is quiet for more than a moment, and drugs 
are more apt to produce extraordinary symptoms as the result 
of idiosyncrasies in this type of patient than in any other, 

The breath of the patient may call the physician's attention to 



GENERAL DIAGNOSTIC CONSIDERATIONS 1 9 

some important facts in connection with the case. If it is sweet 
or vinous in odor, this -may be due to diabetes mellitus; or if it be 
ammoniacal or urinous, uremia may be present. The previous use 
of bismuth may give it a garlic-like smell, due to the contaminating 
tellurium and various aromatic or volatile drugs, such as turpentine 
or copaiba, may be eliminated in the breath. In cases of advanced 
bronchiectasis the breath is often foul, and is insupportably so in 
gangrene of the lung and sometimes when an empyema has rup- 
tured into a bronchus. It is similarly offensive in gangrenous 
stomatitis, and often very disagreeable in tonsillitis. In diphtheria 
it has a peculiarly sickening and sweetish odor. When the odor is 
not dependent on these causes it may be due to ozena, or chronic 
atrophic nasal catarrh, to the presence of decaying food between 
the teeth, or secretions in the crypts of the tonsils. Moderate 
fetor is usually due to disordered digestion and constipation. 

When the physician has gathered as much information as possible 
as to the age and general condition of his patient, by a careful 
scrutiny of his face and extremities, of which scrutiny, however, the 
patient should be unconscious, he should ask him to tell what brings 
him for advice, and, as a rule, this will be the opportunity the 
sufferer seeks to pour out the story of his ailments as he sees or feels 
them. Often the story will seem wearisome, and, to the educated 
mind of the physician, wandering or unnecessary; but to the patient 
every word seems of the greatest importance, and to show any lack 
of interest may give the impression of carelessness, or it may 
interrupt the story just as a most important symptom is about to 
be described. Even if the patient is unable to convey in words a 
very clear idea of his condition, the manner in which his story is 
told, the character of his speech, and the expression of his face 
while speaking may give useful information as to his ailment or 
general state. 

If, instead of the patient being an office or dispensary case, he is 
one who is being visited at home, the fact that the patient meets 
the physician in one of the living-rooms rather than in a bed-room 
indicates either that there is little immediate danger in the case, or 
at least, that the difficulty is not acute, but chronic in type, as 
some slowly progressing form of pulmonary, cardiac, or renal 
disease. Of course, there are exceptions to this rule, as in the case 
of a patient who, having caught a heavy cold, is remaining indoors, 
but not in bed, for prudence's sake. Or, again, if on seeing the 
patient we find him sitting in a chair only partly dressed and 
propped up with pillows, or instead leaning forward upon the back 
of a chair placed in front of him, we know that he is the subject 
most probably of an acute or chronic heart disease, most likely an 
acute exacerbation of the latter. A glance at the face of such a 
patient, revealing a trembling nostril, blue lips, or an anxious 



20 INTRODUCTION 

fades, will aid still further in directing attention to the heart or 
lungs, and the hands, if examined, will appear relaxed and livid or 
darkened in hue, indicating capillary stasis and deficient oxidation 
in the blood. In other cases, however, the patient found sitting 
propped up with pillows may be a convalescent from some Jong 
illness; but if so, the general atmosphere of the patient is better, 
and the surroundings are apt to be more tidy. 

If we find the patient in bed, he may be lying abnormally quiet 
as the result of faintness or acute nausea, or, perhaps, from partial 
or complete coma due to cerebral or renal disease, or from the effects 
of some drug; or, again, he may be rolling about the bed from the 
pain of acute belly-ache, or be keeping his legs and body very still 
while his hands and head are ever on the move to prevent anything 
from suddenly approaching or touching his abdominal wall, as in 
peritonitis. The striking difference between the activity of the 
head and the fixation of the lower part of the body, in peritonitis, 
is notable. Sometimes, however, anxious restlessness indicates 
acute internal or external hemorrhage; but here the movements 
are minute though active, and the patient does not expend so much 
strength as he does when suffering from pain. 

In acute articular rheumatism the patient lies, if many of his 
joints are involved, in a peculiarly helpless position, as if he were 
glued fast to the bed, although the active movement of the eyeballs 
as they follow persons moving about the room gives quite a different 
aspect from that of a patient immovable from stupor. 

Usually a patient who is lying on his side turns on his back 
as the physician or nurse approaches, in order to face his visitor; 
but if he persistently remain on the side without moving, except 
partly to turn his head, we may suspect that in that posture he is 
most comfortable, and that the position is assumed for its comfort 
or to relieve pain or dyspnea, which are suffered from when another 
attitude is taken. Thus, in acute pleurisy the patient lies with the 
affected side uppermost, because it is too sore to permit him to 
touch it to the bed; whereas if the stage of effusion has arrived, he 
lies on the affected side, in order to give the side which is healthy 
free play in compensatory respiratory movements, and to remove 
the pressure of the effusion from the healthy lung. If the patient 
lying in this posture is not suffering from pleurisy, his position may 
be due to an effort to relieve the discomfort caused by an enlarged 
liver. The fact that the patient lies constantly on the back is also 
a characteristic of grave and advanced disease in some instances. 
Very ill persons almost never lie on the side and the fact that a 
desperately ill patient of yesterday is found lying on the side today 
is encouraging. 

Persons with severe heart disease, emphysema, or chronic bron- 
chitis are rarely, if ever, able to lie prone in bed, and have to be 



GENERAL DIAGNOSTIC CONSIDERATIONS 21 

more or less propped up with bed-rests and pillows. Large growths 
in the abdominal cavity producing pressure on the diaphragm also 
necessitate this semiprone posture, and double pleural effusions, 
or pulmonary consolidation or edema, require the upright or half- 
reclining attitude in order that the upper parts of the lung may be 
used to advantage. 

In asthma the patient frequently is found sitting up in bed with 
the arms reaching back of the hips as props to fix the chest and to 
hold the body erect. So too in advanced cardiac and renal disease 
the patient will often take a seat in a chair and rest the head and 
hands on the back of another chair placed in front of him, both 
eating and sleeping in this attitude. 

Again, if the patient wakes when spoken to and then drops off to 
sleep at once, some form of poisoning may be present, as from 
opium, or the poisoning of advanced hepatic or renal disease may be 
present. 

(For the significance of picking at the bedclothes, see chapter 
on the Hands and Arms.) 

The Art of Questioning the Patient. — We can next pass to a 
consideration of the objects to be sought in questioning a patient 
as to the illness from which he is suffering. Often much information 
can be gained by a well-directed question, and a favorable impres- 
sion can be made upon the patient by the manner in which it is put 
and the bearing which it has on his case. Thus, if a man is evi- 
dently much emaciated and his clothes fit him loosely, a question 
in regard to his loss of flesh is very appropriate; but if he is mani- 
festly too stout for comfort such a question will be most unwise. 
Or, again, if a young married woman comes complaining of con- 
stant sickness of the stomach and a fanciful appetite, and the 
physician directs all his questions to the condition of the stomach 
without an eye to a slight increase in size about the waist or below 
it, his professional acumen is in grave danger of being libelled by 
that same woman, who knows, or soon finds out, that her discomfort 
is due to pregnancy. 

If the woman is unmarried and there is no evidence of gastric 
disorder on her tongue, it is well to remember what Battey, of 
Georgia, said in regard to this condition: "Always believe a young 
unmarried woman with abdominal tumor, of high social position 
and unimpeachable virtue, if she has been watched over by a pla- 
tonic and abstemious young cousin of the male persuasion while 
the mother went out, to be pregnant." 

Again, if a married woman of some years tells her physician 
that she has no children, the physician naturally asks some ques- 
tions which elicit the fact that she has had frequent miscarriages. 
He in this way finds out quite as much about probable syphilitic 
infection as if the question had been put: "Have you ever had a 



2 2 INTRODUCTION 

sore on your privates?" which would embarrass the patient, produce 
domestic troubles, and probably be lied about if her husband is 
forced to answer the question. 

Again, when asking a woman about the health of the living 
parents, or the cause of death of the dead, care should be taken 
not to ask a direct question, as, for example, whether the mother 
has died of cancer, for the patient may be already greatly worried 
lest she has that disease. It is better to ask the cause of death, or 
of the illness she is suffering from. If the story is that the parents 
died of "bronchitis," the real cause of death was probably tubercu- 
losis of the lungs. 

If the patient complains of pain, past or present, the best way 
in which to discover its true seat is to ask him to place his hand on 
the affected part, as in this way errors in his description of his 
anatomy will not be committed, and false impressions will not be 
conveyed to the physician's mind. Even this direct method, of 
showing the area of pain is not to be absolutely relied upon, for 
often pains are referred to parts in which there is no disease. Thus, 
the pain of coxalgia is apt to be felt in the knee and ankle, and in 
children the pain of pulmonary or cardiac disease is often described 
by the patient as felt in the abdomen. If the pain has been really 
abdominal, there will, in many cases, have been diarrhea or free 
passage of flatus. It is not to be forgotten, on the other hand, that 
a question which discovers the fact of several movements of the 
bowels does not prove the presence of true diarrhea, because a 
purgative may have been taken by the patient. 

In asking questions as to constipation, the physician must not 
forget that the opinion of the patient as to what constitutes regu- 
larity of bowel movement is of very little value in many instances. 
A daily movement is not known to many patients, and a movement 
every few days may be quite sufficient to justify the statement, in 
their opinion, that no constipation is present. 

The young physician, in particular, in asking questions of women 
patients of the better class, should not hesitate to ask direct ques- 
tions as to the state of the bowels or of the menstrual function. To 
hesitate or ask indirect questions about such matters simply pro- 
duces embarrassment which otherwise would not exist, and inti- 
mates that the question is one of doubtful propriety, when in 
reality it is most important and proper. 

The Examination of Children. — If the patient to be examined is a 
child, it is well for the physician to remember that his presence as a 
stranger may be a source of alarm, and that the association in the 
child's mind of sickness and the doctor, and badly tasting medi- 
cines, is sufficient to render him a much-to-be-dreaded individual. 
Generally it is best, on entering the room where the child is, to 
pretend to pay no attention to it whatever, but to engage in con- 



GENERAL DIAGNOSTIC CONSIDERATIONS 23 

versation with the mother or other person, speaking of the case in 
a way which the child will not understand. Very often this very 
lack of attention will result in the child forcing the recognition 
of his presence upon the physician by making the first advances 
toward friendship, and this is particularly apt to be the case if the 
child is already spoiled by overattention by the family and friends. 
Time should always be given the child to grow accustomed to the 
peculiarities of the visitor, and if any instrument for diagnosis is 
to be employed it is best to hold it in the hand as if it were a play- 
thing before attempting to put it into actual use. The tact which 
the physician must exercise in diverting a sick child is essen- 
tial to the successful treatment of children. Some physicians are 
welcomed to a house by the sick and well as Santa Claus would be, 
and others, devoid of the trait of amusing children, are fled from 
as if they were dragons. 

During the time that the physician is allowing the child to get 
accustomed to his presence he should be gaining much useful infor- 
mation about the case by observing the movements and expressions 
of the child; its color, size, nutrition, breathing; the shape and size 
of its head; the condition of its lips, whether moist or dry, red, livid, 
or pale; and, if the child is speaking, the tone of its voice, or, if 
crying, the character of its cry. It is needless to state that a child 
may cry from fright, pain, anger, or hunger. Constant screaming 
is, however, nearly always due to the pain of earache or hunger, 
for abdominal colic is usually intermittent. If there be pain in 
the ear, the hand will often be rubbed over the affected side of the 
head, and the child will not be pacified by the offer of the breast. If 
the child coughs, and then rjegins to cry, pneumonia or pleurisy 
may be present; or in other cases the pain is so great that the 
child is cryless. A sharp, piercing shriek indicates the pain of 
earache or of meningitis in many cases. (See chapter on Head- 
ache.) 

If a crying child be placed at the breast, which it takes with 
avidity only to drop the nipple in a moment with a cry of pain or 
anger, one of several conditions is present: either the child has 
stomatitis or the breast is empty; or, again, if it seizes the breast 
and then lets go with a gasp, it may have coryza or syphilitic 
snuffles, which prevents it from breathing through the nose while 
sucking. Similar signs may be present in any other condition pro- 
ducing shortness of breath. 

If a child over four months of age cries and sheds no tears in 
the course of an illness, this is an unfavorable sign. 

It is important to notice whether there is languor or a tendency 
to play. A healthy infant, when awake and well fed, is always 
kicking^ and cooing and moving its arms about, and has a happy 
expression on its face; whereas if any cerebral trouble is present 



24 INTRODUCTION 

it often has an anxious frown, or its hands are placed on the side 
of its head or rubbed over the vertex. 

In a perfectly healthy child which is sleeping, the respiration 
should be practically inaudible, and it is a good practice to note the 
regularity of the breathing in all patients while they are asleep, 
as it is then unaffected by voluntary effort. In children a sighing 
breathing, or one disturbed in rhythm, often indicates a disturbed 
digestion or fever. 

The physician should always, by careful questioning of the nurse 
or mother, find out how long the illness has lasted, the manner in 
which it began, the fact as to whether a similar attack has occurred 
before in this or other children of the family, and the state of the 
temper, appetite, bowels, and urine of the patient, for an irritable 
temper in a child means ill health, as does also a poor appetite, 
constipation, diarrhea, or abnormal urine. 

The expression of the face, shape of the head, and similar note- 
worthy points in the diagnosis of the case will be more thoroughly 
discussed in the chapter devoted to these parts. (See chapter on 
the Face.) 

When it comes to a close examination of an infant, great care 
must be exercised. The character and rapidity of the respirations 
are best studied at a distance before excitement has disturbed them, 
and the best way to listen to a young child's chest is when it is 
held over the shoulder of the mother, as if she were carrying it for 
a walk, or, if the infant can be taken in the physician's arms, its 
buttocks should rest on one hand, while the front of its chest rests 
against the other. In this way the physician can listen to the back 
of the chest without difficulty, keeping the child amused by walk- 
ing up and down the room while it is in his hands. 

If it is not possible by any bribe to cause the child to protrude 
the tongue for examination, the physisian will often be able to see 
this organ when the mouth is widely opened in crying. 

In taking a child's pulse it is best to take it while it is asleep, if 
possible, as the excitement of the physician's visit or the crying on 
awakening will greatly increase the pu]se-rate. 



CHAPTER I. 
THE FACE AND HEAD. 

The expression and color of the face — Facial deformity — Facial paralysis, 
unilateral and bilateral — Ptosis — Facial spasm — The shape of the head — 
The movements and position of the head and neck. 

So much can be learned by the physician from the expression and 
general appearance of a patient's face and the carriage and shape of 
his head that a careful inspection of these parts should always be 
made. For this reason, in the consulting-room and at the bedside, 
the physician should always arrange his chair in such a way that 
the light falls upon the face of his patient, while his own is in 
the shadow, and this is of importance not only because the facial 
expression of the patient can thus be well seen, but also because 
it prevents the patient from making a too close scrutiny of the 
physician's face with the object of detecting encouragement, lack 
of sympathy, or alarm. 

THE FACE. 

The Expression. — The expression is produced by the formation of 
creases, or alterations in the contour of the skin and subcutaneous 
tissues by trophic and muscular action, and these changes are in 
time brought about and perhaps made permanent by the mental 
tendencies and habits of the patient, his temperament, his intel- 
lectual development, his exposure to outdoor or indoor influences, 
and, finally, and these are very important, by pathological processes 
which may be going on somewhere in his body. The temper of 
the man also affects his expression, particularly as he approaches 
middle life, and he looks amiable, capable of sudden anger, or 
sullen, as the case may be. 

The intellectual face is easily recognized. Sometimes it is deeply 
thoughtful and placid, at others eager or keenly alive to the sur- 
roundings or the conversation, and it separates the man descended 
from several generations of men who have lived as thinkers from 
him whose ancestors have been but recently wage-earners by 
physical labor, involving only ordinary human intelligence. 

The skin of the face and the expression about the eyes of one 
who has been exposed for years to the weather are so characteristic 



26 THE FACE AXD HEAD 

as to need no description, while the face of the clerk, whose life is 
almost entirely spent indoors, is pale and wan. 

Fulness of the lips, particularly of the lower lip, is supposed to 
be present in persons of strong sexual appetite, and often indicates 
a phlegmatic temperament, whereas the thin, mobile lip is typical 
of the high-strung, nervous individual. 

The expression of the lips as a whole is also to be regarded in 
connection with the expression of smiling. The risus sardonicus 
of strychnine poisoning or tetanus is quite characteristic, and the 
simple smile of hysteria is equally notorious. 

Similarly, the face of a person who uses alcohol to excess is 
generally flushed, heavy, and more or less expressionless. The 
eyelids are redder than normal, and the skin is apt to be puffy and 
unhealthy looking. Women at the menstrual period, or when 
suffering from menstrual disorders, often have dark areas under 
the eyes, and pigmentation of the eyelids is often seen very early in 
pregnancy. In women, and sometimes in men, excessive fatigue 
and loss of sleep cause marked infra-orbital discoloration. A 
puffiness under the eyes, most noticeable in the morning, may indi- 
cate renal lesions or the excessive use of arsenic; or if it is unilateral 
it probably depends upon some local inflammation of the eye or 
rarely upon disease of one of the cephalic sinuses. So, too, an 
ecchymotic spot under the eye may be due to a bruise, to some one 
of the forms of purpura, or to scurvy. 

The color of the face is discussed in the chapter on the Skin, but 
it is not out of place to note at this point the pallor of the face in 
fright, faintness from hemorrhage (acute or chronic), that due to 
lack* of proper food, and the peculiar pallor of chlorosis. In the 
latter disease the faint yellowish-green tinge of the skin in some 
parts of the face, which still retains its plumpness, is quite typical. 
A parchment-like skin stretched over the face so that it appears as 
if stretched and dried over the under structures is seen in some 
young persons suffering from syphilis, and in some cases of advanced 
hepatic cirrhosis. 

The color of the face may be rendered gray or bluish by the 
ingestion of overdoses of the coal-tar products, such as acetanilid, 
antipyrine, and phenacetin, and it is curious that this effect is best 
seen when the patient is viewed at a little distance. (For the signi- 
ficance of facial cyanosis, see chapter on the Skin.) 

In view of the extraordinary variations seen in the expression of 
the face in the healthy it is not surprising that this part of the body 
should give the physician, when studying disease, so much useful 
information. It is an interesting fact, too, and one not unworthy 
of note, that the. true facial expression of a disease is rarely aped by 
a malingerer, and in all diseases is unrecognized by the patient even 
though he sees himself several times daily in a looking-glass. Thus 



THE FACE 27 

it is by no means uncommon to see a person who is suffering from 
the onset of some sudden and grave disease bearing upon his face 
what we call "an expression of anxiety," when he himself as yet 
has no conception of the gravity of his illness. This expression is 
very characteristic of serious illness, and, though difficult to describe, 
when recognized becomes quite valuable as a diagnostic factor, 
particularly as it rarely, if ever, is exaggerated by the patient who 
bears it. It is seen most markedly in cases of severe acute croupous 
pneumonia, in peritonitis, or after severe injuries. 

When persons have had continuous pain for a long time, as in 
patients who have growths of a malignant character or other organic 
disease, the expression of the face, naturally gentle, often becomes 
hard and stony, or if the pain be in the head, the expression, is not 
only that of pain, but of profound mental depression. In cases of 
visceral carcinoma the face becomes thin, its skin yellow and straw-' 
colored, and oftentimes greasy and thick, and there is often a 
marked expression of anxiety. On the other hand, the patient 
sometimes has a dogged expression on his face as if he had been 
told of the true cause of his illness, and was rebelling against the 
inevitable progress of the disease. 

In the case of children, much information can be gained as to the 
state of the system by the facial expression, particularly while the 
child sleeps. If it is asleep and healthy and well, the eyelids are 
closed, the lips are never so slightly parted, the nostrils are prac- 
tically immobile, and the general expression is very peaceful. If, 
on the other hand, the eyelids of a sleeping child are slightly parted 
so as to show the whites of the eyes, there is probably present some 
digestive or nervous disturbance, perhaps accompanied by moder- 
ate pain. If in the course of an illness the eyelids remain far 
enough apart to result in glazing of the conjunctiva from dryness, 
this is a sign of grave import. Again, twitching of the eyelids often 
indicates nervous irritation or the early stages of the convulsive 
state, and it is not uncommon for an expression to pass over the 
face of a child who, while sleeping, is suffering from pain, which 
begins as a smile and ends with a drawing-in of the corners of the 
mouth, an expression somewhat like that seen on the face of a 
waking child when it seems to be in doubt as to whether to laugh or 
to cry. Whether asleep or awake a child in pain, if not crying, has 
a pinched look about its nose and mouth, and sometimes some idea 
of the seat of the pain may be gained by the part of the face which is 
drawn. When pain is in the head, the forehead is apt to be wrinkled 
into a frown; if the nose is pinched and drawn, it is said to show that 
the pain is in the chest; and if the upper lip is raised, pain is probablv 
felt in the belly. 

Aside from these symptomatic manifestations, however, we find 
in the face of a child several evidences of important diathetic tend- 



28 THE FACE AND HEAD 

encies, or even hereditary diseases. Thus we see the light flaxen- 
haired, slimly built child with a refined, spirituelle face and trans- 
parent skin, whose temporal veins can be easily traced and whose 
expression is often thoughtful and deep. Such a child often comes 
of tuberculous parents, and is frequently a victim of tuberculosis, in 
one of its rapid forms, as it approaches puberty. Or, again, the 
child is " stocky" and cheesy looking, apparently solid and sturdy, 
but its features are heavy or perhaps even coarse, while its neck is 
thick and short. Such a child is often a victim of tuberculous 
bone or lymphatic disease. In other instances a square, projecting 
forehead with faulty bone development elsewhere indicates rickets, 
or an immense, bulging forehead with a wizened, puny face beneath 
shows hydrocephalic tendencies. Sometimes a broadness of the 
bridge of the nose or marked flatness of it indicates congenital 
syphilis. Such a child is often much wasted, its features pinched, 
and its lips thin, while the flattened nasal bridge is bluish, and its 
face is often that of a little old man, shrivelled and wrinkled. 
Mucous patches at the corners of the mouth or around the anus 
are often found in such cases, and, if found, confirm the diagnosis 
of infantile syphilis. 

In children suffering from lesions of the mitral valve of the heart 
it is very common for some blurring or indistinctness of the 
features to be present. 

Finally, in respect to facial expression in childhood, attention 
must be called to the "fish mouth," vacuous and "nose-pinched" 
expression of those children who are "mouth-breathers" from nasal 
obstruction (Fig. i). 

Great immobility of the lips and cheeks may be due to mucous 
patches or other ulcerations of the buccal mucous membrane; and 
if high fever is present, the presence of herpetic blisters about the 
lips points to the possible presence of croupous pneumonia in the 
child or adult. 

The face of a patient with acute fever is apt to be red and flushed, 
and the eyes bright; and if the disease be distinctly infectious, as in 
some cases of pneumonia, tuberculosis, and acute articular rheuma- 
tism, it may be covered with sweat. 

The facial expression of adults in many diseases is even more 
characteristic than it is in children. Thus, we see in acute pul- 
monary phthisis the widely opened eye, the hunted expression, the 
quivering nostrils, the red flush over the malar bones, the wasting 
and dryness of the hair and skin, and the eager or in other cases 
apathetic glance of the eye. 

In severe croupous pneumonia the flushed face, with a deeper red 
on one cheek than the other, the anxious expression, and the dilated 
nostril are noteworthy; and in the dyspnea of heart disease the 
dilated nostril and constant opening of the mouth, as if seeking for 



THE FACE 



2Q 



air, with the facial pallor or cyanosis, are characteristic. Often, 
too, in chronic cardiac or pulmonary disease producing slight diffi- 
culty in respiration, the patient's lips are seen to be slightly parted 
and dry, and may appear somewhat cyanotic. 

One of the most characteristic facial expressions that we meet 
with is that of typhoid fever or fevers of a typhoid type. The face 
is dull and expressionless; the teeth are covered with sordes, which 
become brown and blackish by exposure or by discoloration from 
medicines and foods; the lips are often moved in a low muttering 
delirium; and the whole appearance is that of apathy. Even when 
spoken to, the face of a patient suffering from enteric fever rarely 
lights up in response to the greeting. 




Fig. i.— Mouth breather, from obstruction of the nasopharynx; open mouth; 
vacant expression; pinched nostrils; dull eyes; drooping eyelids; round 
shoulders 



Equally, if not more, characteristic is the facial expression of 
acute peritonitis. The upper lip is drawn up in such a way as to 
show the teeth, and the expression of anxiety and nervous unrest 
is well developed. Similarly in abdominal pain due to other causes 
than peritonitis there is often a twitching of the muscles of the lip 
and about the eye which is quite typical. This twitch is said by 
Fothergill to be peculiar to pain below the diaphragm, and he is 
also responsible for the statement that it is best seen in the face of 
the parturient woman in the second stage of labor. 



3Q 



THE FACE AND HEAD 



The facial expression of hysteria may be apathetic, or it is that 
of devotion, rage, or grief, and these expressions are fixed if the 
patient be cataleptic. If she is not cataleptic, not infrequently one 
expression may succeed the other, or in their place there conies that 
curious smile or vacuous expression of the face which is so char- 
acteristic. It should be remembered, however, that this vacant, 
fatuous look may occur in women suffering from the early stages of 
disseminated sclerosis and in children with chorea. Then we have 
the elated facial expression of general paralysis of the insane, the 
excited look of acute mania, the beaten, weary, careworn look or 
apathetic glance of nervous exhaustion, and the hopeless expression 
of melancholia. 




Fig. 2. — Face of a patient with general anasarca due to chronic parenchy- 
matous nephritis. (From a patient in the author's wards, Jefferson Medical 
College Hospital.) 



The face of paralysis agitans, sometimes called the " Parkinsonian 
visage," is distressed and pathetic, and yet somewhat intense. (See 
chapter on the Hands and Arms, that part on Tremor.) 

A pale, puffy face, generally looking worn and weary, may be seen 
in cases of chronic or subacute renal disease. In children there is 
often in this condition a peculiar transparent or pearly look in the 
lower eyelid, so that it seems somewhat pellucid. Great swelling 
or edema of the face is seen in erysipelas, dropsy (Fig. 2), and simple 
inflammatory swelling. (See chapter on the Skin.) In trichiniasis 



THE FACE 31 

the eyelids are often swollen early in the disease, and then recover 
their normal appearance only to become swollen again later in the 
malady. 

The facies of exhausting disease about to produce death is very 
characteristic, and is seen frequently in cholera and in tuberculosis 
of the lungs or any state associated with profound collapse, such as 
internal hemorrhage. It is accompanied by pallor, cold extremities, 
and difficult breathing. This is called the "Hippocratic face," and 
is peculiar in the sinking-in of the temples where the jaw muscles 
are inserted; the eyes are sunken, and around them are great 
hollows, so that the infra- and supra-orbital ridges become greatly 
accentuated. The eyelids are slightly parted, the cornea somewhat 
glazed; the nose pinched, its skin drawn; and the lower jaw some- 
what dropped. Such a facial expression, if typical, is a sure fore- 
runner of dissolution. 

When the face bears a sleepy, listless expression, the forehead 
being devoid of wrinkles, and there are present faulty movements 
of the lips, which cannot be approximated, as in whistling, and at 
the same time the patient is unable to close the eyes entirely, 
although the lids droop, the physician should think of the possi- 
bility of these being the early symptoms of what has been called 
the "faciohumeroscapular" type of muscular atrophy. (Landouzy 
and Dejerine.) The disease, as its name implies, speedily involves 
the scapulae and arms after affecting the face, and exophthalmos is 
often present. This form of muscular atrophy lacks the fibrillary 
twitchings seen in spinal progressive muscular atrophy, and there 
are no changes in electrical excitability, except that owing to the 
loss of muscle fibre the reaction is feeble. The facts that more than 
one member of the family is affected and that the disease is of long 
duration, added to these signs, render the diagnosis easy. It is a 
very rare disease. 

An appearance of the face almost identical with that just de- 
scribed is seen in Friedreich's ataxia, and is often one of the earlier 
manifestations of the disease; but the presence in Friedreich's ataxia 
of the ataxic gait, the jerky articulation, nystagmus, loss of knee- 
jerks, and absence of muscular atrophy separate it from the 
Landouzy-Dejerine type of muscular atrophy just described as 
faciohumeroscapular atrophy. (See Ataxia in chapter on the Feet 
and Legs.) - 

The facial expression of cretinism is exceedingly characteristic. 
The nose is broad and flat, the eyelids are swollen, the lips greatly 
thickened, and the enlarged tongue lolls out of the mouth, from 
which saliva constantly dribbles, while the waxy skin and subnor- 
mal temperature of the body, with a poor circulation, slow respira- 
tion, and mental hebetude, complete the symptom group. There is 
nearly alwaysin well-developed cases marked lumbar lordosis (Fig. 3) . 



32 



THE FACE AND HEAD 



The facial expression of myxedema is heavy and listness, as a 
rule. (See chapter on the Skin.) 

In certain forms of leprosy the face often becomes leonine, or 
lion-like in appearance. 




Fig. 3. — A cretin. (Dercum.) 



Facial Deformity. — Facial asymmetry is sometimes seen as a 
congenital defect, and curiously enough is often developed in 
children who suffer from congenital wry-neck. This is not to be 
confused with that extraordinary affection called facial hemiatrophy 
which usually begins in childhood in one spot, and slowly proceeds 
until one side of the face, sharply outlined from the other, becomes 
wasted in its skin, muscles, bones, color, and hair. Even the eye 
may be sunken and shrunken. Rarely this wasting extends over 
the whole of one side of the body, and still more rarely is bilateral. 

Sometimes in facial hemiatrophy the wasting is accompanied by 
painful twitchings, which increase with mental excitement. More 
rarely there is decrease in the acuity of taste and hearing on the 
affected side, while myosis, sweating, or excessive dryness of the 
skin may also be found on this side. Such symptoms as the last 



THE FACE 



33 



show involvement of the sympathetic nerve fibres. The changes 
are probably due to disease of the fifth (trifacial) nerve. 

As to whether circumscribed sclerodema (morphea) and facial 
hemiatrophy are identical — -that is, whether the first is a well-devel- 
oped form of the latter — is not decided. Hyde apparently regards 
them as identical. (See chapter on the Skin, Scleroderma.) 




%.. 



oh 




Fig. 4. — Acromegaly, showing the large face and hands. (Dercum.) 



Even more rare than facial hemiatrophy is facial hemihyper- 
trophy, one side remaining normal in size and the other becoming 
gigantic. 

The massive face of a person suffering from acromegaly is very 
characteristic (Fig. 4). 

The face has a full-moon broadness in myxedema. The enlarge- 
ment of the bony parts of the skeleton, the kyphosis, and the 
comparative muscular feebleness of acromegaly aid in the diagnosis 
of that disease, for in myxedema there is no true bony enlargement. 

The face in osteitis deformans is shaped like a triangle with the 
base upward, the shafts of the long bones become weakened, and 
3 



34 THE FACE AND HEAD 

their surfaces roughened from periosteal deposits. (See chapter 
on the Hands and Arms.) 

Unilateral Facial Paralysis. — Very notable changes in the face are 
produced by paralysis, the palsy being, as a rule, unilateral and 
depending upon central or peripheral nerve lesions for its cause. 
Smiling, when unilateral paralysis is present, results in the drawing 
back of only one corner of the mouth (on the well side), and whist- 
ling or the pronunciation of labia] sounds is difficult or impossible. 
The cheek of the paralyzed side is often puffed out with each expi- 
ration, but the wrinkling of the skin is on the side of the face which 
is not paralyzed, owing to contraction of the muscles which are 
unopposed. (For a description of the general anatomy and physi- 
ology of the nervous tracts involved in paralysis of the face and 
elsewhere, see chapter on Hemiplegia.) 

Unilateral paralysis is, as already stated, the form of facial par- 
alysis most commonly seen, and is generally due to injury of the 
facial nerve trunk. The lesion producing the paralysis may be 
peripheral — that is, in the nerve itself — or central, that is, in the 
pons or the cerebral cortex. The former variety is the most com- 
mon, provided the paralysis is purely facial, and it is usually due to 
inflammation of the nerve sheath as it passes through the stylo- 
mastoid foramen, the loss of function being due to pressure on the 
axis-cylinders owing to the presence of swelling in so limited a canal. 
Such an attack will generally be found associated with a history of 
exposure to cold or injury by a blow, or with that of middle-ear 
disease with caries of the petrous portion of the temporal bone follow- 
ing otitis, which inflammatory process causes pressure on the nerve. 
It is not necessary for the otitis to be suppurative or for caries to 
exist in all cases, for it seems probable that by the extension of 
inflammation along the chorda tympani such a paralysis may 
result. If the disease be in the petrous portion of the temporal bone, 
in addition to paralysis of the muscles of expression there will also 
be loss of taste in the anterior part of the tongue due to involvement 
of the chorda tympani, the mouth is dry, owing to a lack of saliva, 
the salivary gland being paralyzed, and there may be deafness from 
paralysis of the stapedius muscle. Still more rarely facial paralysis 
results from swelling of the parotid gland or from a tumor in its 
neighborhood, and it may occur as the result of pressure by growths 
at the base of the brain, syphilitic or otherwise, from fracture of the 
base of the skull involving the petrous portion of the temporal bone, 
and very rarely, when the disease occurs in the newborn, from 
hemorrhage from the cerebellum during birth, or from pressure by 
forceps. (See below.) Finally, paralysis due to a peripheral lesion 
of the nerve may result from neuritis, and from primary hemorrhage 
into the nerve sheath or into the stylomastoid canal. Facial 
paralysis may also arise from locomotor ataxia, the lesion being in 



THE FACE 35 

the pons, and from hysteria. All these forms are very rare, com- 
paratively speaking. The cerebral or medullary lesions which 
produce unilateral facial paralysis usually result from hemorrhage 
and tumor. 

The determination that facial paralysis is due to a peripheral 
neuritis or pressure may be impossible at the first visit of the patient, 
if this visit is made, as it usually is, within a few hours of the onset 
of the malady; but the peripheral form separates itself from facial 
paralysis of cerebral origin in the course of ten days or two weeks, 
for, if the nerve is inflamed or pressed upon in the foramen, the 
muscles of the face speedily undergo degeneration, because they 
are cut off from their trophic centre. 

In the cerebral form, on the other hand; the trophic changes do 
not occur, and the reactions of degeneration fail to appear, because 
trophic impulses can still reach the facial nerve trunk and the 
muscles which it supplies. In other words, electrical response in 
the paralyzed side remains normal in centric lesions and is lost 
in peripheral lesions. The only other conditions in which there 
can be developed the reaction of degeneration and the lesion not be 
in the nerve trunk or foramen is when there is a tumor at the 
base of the brain involving the facial fibres below the facial nucleus 
or destroying the nucleus itself. 

Very rarely in cerebral facial paralysis is the loss of power as 
complete as it is in the peripheral form. Again, in cerebral facial 
paralysis the eye on the paralyzed side can usually be closed and 
the forehead wrinkled, whereas in the peripheral form it cannot. 
Why this should be so is not clear, unless it is that in the muscles 
used commonly in pairs, as in those of the forehead, there is an 
adequate nerve supply through direct non-decussating tracts which 
innervate the muscles. 

When facial paralysis has associated with it none of the signs of 
peripheral wasting, and none of the remote causes of hemorrhage, 
embolism or thrombosis, such as result from impaired bloodvessels 
or a diseased heart, and when the paralysis comes on gradually 
(though it may be sudden from surrounding inflammation), the 
condition is probably due to cerebral tumor. This diagnosis is 
confirmed by the gradual spread of the paralysis to other parts, as 
the arm and then the leg on the same side of the body, and by the 
development, often before each additional spread of the paralysis, 
of a convulsion. 

The facial paralysis resulting from tumor at the base of the 
brain differs from that due to cerebral tumor or hemorrhage, 
by^ the fact, already stated, that the reaction of degeneration 
quickly develops in the paralyzed part; that the parts supplied 
by the upper branch of the facial are often quite as much par- 
alyzed as are those supplied by the lower branch, which is rare 



36 THE FACE AND HEAD 

in the cerebral lesion; and there will commonly be found other 
evidences of a growth which, in a region so densely filled with 
important centres, speedily affects other functions. Thus in asso- 
ciation with this form of facial paralysis there will nearly always 
be found paralysis of the oculomotor nerve, causing ptosis, a mod- 
erately dilated pupil, and external squint, and there may also be 
paralysis of the abduceris or sixth nerve, which causes internal 
squint by paralysis of the external rectus muscle. (See Ptosis.) 
The optic nerve may show choked disk, and there may be disturb- 
ance of vision. (See chapter on the Eye.) If the tumor is large, or 
is so placed as to involve the facial fibres for both sides as well as 
those of the oculomotor, abducens, and optic nerves on both sides, 
all these symptoms become, of course, bilateral. 

Facial palsy associated with deafness may indicate cerebellar 
tumor, the diagnosis of this cause being decided by the other cere- 
bellar symptoms, such as the peculiar gait. (See chapter on Feet 
and Legs.) Such growths are not uncommon in children. 

Sometimes very shortly after birth the child is seen to have a 
facial paralysis resulting from pressure by the forceps, which have 
slipped and injured the facial nerve, or have caused an extravasation 
of blood into the neighborhood of the parotid gland, thereby causing 
pressure on the nerve. The prognosis is usually favorable if due 
to such causes; but if the forceps have caused facial palsy by pro- 
ducing a cerebral hemorrhage, the outlook is bad. 

The possibility of facial paralysis being due to hysteria should 
not be forgotten. The loss of power under these conditions may 
be unilateral or bilateral, generally the former. Its association with 
the symptoms of hysteria described in the chapter on the Skin, and 
elsewhere in this book, will aid in making the diagnosis. 

There yet remain to be considered several forms of facial paralysis 
unilateral in character yet associated with paralysis elsewhere. 
These are as follows: 

Unilateral facial paralysis very rarely occurs in association with 
monoplegia in acute anterior poliomyelitis. So seldom does it occur 
in this connection that it has been denied an existence. Often it 
is but temporary, while the monoplegia of the arm is permanent. 
It occurs more commonly with the disease in adults than in 
children. 

Facial paralysis with arm paralysis of the same side, followed in 
a short time by paralysis of the leg of the opposite side, is quite a 
characteristic symptom of syphilitic arteritis at the base of the 
brain. 

Crossed paralysis — that is, paralysis of the face on one side, and 
of the arm and leg on the other — is due to a lesion in the pons above 
the decussation of the pyramids and below that of the facial fibres 
(Fig. 5) . Thus it is seen in this figure, on the left side, third inscrip- 



THE FACE 



37 



tion, that the lesion in the pons cuts off the motor fibres in the 
place indicated, thereby causing the distribution of the paralysis 
just named. (See also chapters on Hemiplegia and on the Arms 
and Hands.) 



Lesion of cerebral mo- 
noplegia (brachial) 



Lesion of ordinary 
hemiplegia 



Lesion of cross paralysis 
(face of same side toith 
limbs of other side) 



A lesion causing paraplegia 



A lesion causing hemi- 
paraplegia 




Cortical centre for op- 
posite leg 



Cortical centre for op- 
posite arm 



Cortical centre for op- 
posite side of face 



Internal capsule (pos- 
terior limb) 



Motor nerve to face 



Decussation of pyra- 
mids 



Crossed pyramidal tract 



Motor nerves to upper 
limb 



Crossed pyramidal tract 



Sensory nerves entering 
cord, and decussating 
soon after entry 



Motor nerves to lower 
limb 



Fig. 5. — Diagram to show the general arrangement of the motor tract 
and the effect of lesions at various points. (Ormerod.) 



Sometimes the muscles supplied by the facial nerve escape par- 
alysis, but those of the jaw — namely, the masseters and temporals — 
become paralyzed either bilaterally or more commonly unilaterally. 
This is a rare affection, and depends upon paralysis of the inferior 
maxillary branch of the trifacial nerve. This may be due to 
pressure produced by growths or inflammatory processes at the 
base of the skull. It may also occur as the result of hemorrhage 
into the medulla, or from progressive bulbar paralysis. 



38 THE FACE AND HEAD 

Ptosis. — In connection with the subject of facial paralysis that 
of ptosis, or drooping of the upper eyelid, must be considered. 
It depends upon loss of function of the oculomotor nerve or its 
nucleus. Ptosis is a symptom of the greatest importance, first, 
because it is so readily recognized; second, because it is a source of 
great annoyance and alarm to the patient; and, third, and more 
important, it often aids us greatly in localizing lesions. 

The presence of this symptom should call to the physician's mind 
the various causes which produce it. In the first place it sometimes 
occurs as a congenital defect, and in such a case the history of the 
patient renders the diagnosis easy. 

If a congenital defect is not responsible for the ptosis it must 
depend upon disease affecting the oculomotor nerve itself or its 
nucleus. If the disease be sufficient to cause entire loss of 
function, we find, in addition to ptosis, that there is paralysis 
of all the external muscles of the eye except the superior oblique 
and external rectus, and in addition there will be a moderately 
dilated pupil, which wi]l not contract, and paralysis of the 
ciliary muscle — that is, loss of accommodation. The eye can be 
moved outward by the action of the external rectus, and a little 
downward and inward by the superior oblique. Diplopia is 
present, and a little exophthalmos may be present, owing to the 
action of the superior oblique, which presses on the ball. If the 
lesion be in the oculomotor nucleus, the near position of the nuclei 
of the fourth and sixth nerves will probably cause them to be 
affected also, thereby causing a general ophthalmoplegia (Fig. 6). 
If the lesion is not nuclear it is due to disease in the nerve itself, 
as already pointed out. If this is the case the lesion is probably 
due to pressure in the cavernous sinus or to periostitis of the bones 
forming the sphenoidal fissure through which the nerve passes. 
(See Plate I.) Sometimes, however, the paralysis of the nerve may 
be only partial, so that the external muscles of the eyeball escape, 
and only ptosis and a dilated pupil are present. 

Very rarely ptosis results from a cerebral hemorrhage, without 
the other signs of oculomotor paralysis being present. That is to say, 
the branch of the oculomotor which supplies the levator palpebral 
is affected, while the branches supplying the external and internal 
ocular muscles escape. 

If there is a history of a cerebral attack resembling a mild apo- 
plexy, and a unilateral ptosis is present, the lesion is probably in 
the cortical centre for the oculomotor nerve in the angular gyrus 
just below the interparietal fissure. The lesion is, of course, upon 
the side of the cortex opposite the ptosis. Such a cause is very 
rare. 

A fourth cause of ptosis is due to an affection of the sympathetic 
nerve, and is sometimes called pseudoptosis. There are associated 



PLATE I 




Base of Skull, showing the Oculomotor Nerves (III) Passing through the 
Sphenoidal Foramen. (Modified from Arnold.) 

The other cranial nerves are also numbered, and it is easy to see how an inflammatory exudate 

at the base might involve many of them. 

III. The oculomotor nerves. IV. The pathetic nerves. V. The trifacial nerves. 

VI. Abducens. VII. The facial nerves. 



THE FACE 39 

symptoms of vascular dilatation, with redness and swelling of the 
skin of the affected side, elevation of temperature in that part, con- 
traction of the pupil on the affected side, and apparent shrinkage of 
the eye into the orbit. This form of ptosis results from the paralysis 
of the unstriped muscular fibres of Miiller which exist in the orbital 
fascia, and as these muscular fibres aid in holding open the lid their 
paralysis results in partial ptosis. Nothnagel asserts that such 
symptoms occur with lesions in the corpus striatum. 




K J "' 




Fig. 6. — Showing the nearness or origin of the oculomotor (3), pathetic (4), 
and adducens (6). The roots of these nerves are shown by an incision which has 
divided the pons. III. The third nerve, arising from several roots. IV. The 
fourth nerve. VI. The sixth nerve, arising from three roots. (Modified from 
Arnold.) 

A fifth cause of ptosis is reflex irritation usually through the 
fifth nerve. This is probably due to an inhibition of the oculomotor 
centre. It is usually only transient. 

Sixthly, it is not uncommon in cases of nervous syphilis for 
so-called alternate ptosis to develop. First one eye is affected 
by ptosis and then the other just as the first begins to improve 
or recover. 



40 THE FACE AND HEAD 

Ptosis has been known to complicate tetanus, probably as the 
result of reflex irritation of the fifth nerve. 

Ptosis, either unilateral or bilateral, may arise from hysteria and 
idiopathic muscular atrophy. If from hysteria the diagnosis can 
be made from the age, sex, and history of the patient, from the 
presence of hysterical sensory changes described in the chapter on 
the Skin, and from the fact that there is a tendency to spasm of the 
orbicularis muscle when the patient is made to look up. This con- 
traction of the orbicularis proves that there is no true paralysis of 
the levators. If the ptosis is bilateral and hysterical the head is 
tipped back when the patient is told to look up. 

Single or double ptosis is by no means a rare symptom of loco- 
motor ataxia, and is often associated with other evidences of oculo- 
motor palsy. Sometimes diplopia due to this disease is the first 
symptom complained of, and the patient may state that the 
diplopia comes and goes. 

Bilateral ptosis, like unilateral ptosis, may arise from tuberculous 
or syphilitic changes about the base of the brain owing to pressure 
on the cranial nerves (see Plate I), or it may be congenital, or if 
transient be caused by poisoning by gelsemium or conium. It is 
also seen in slight degree in feeble, overworked women, particularly 
in the early morning on awakening. 

Again, it is not very rare to see slight drooping of both lids in all 
the members of a family, in which case the condition is usually most 
marked in the women, and is to some extent combated by the frontal 
muscles, which, in contracting, make the patient frown and draw up 
the eyebrows. (See chapter on the Eye.) 

Ptosis, with hemiplegia of the face and limbs, on the opposite side 
of the body, associated it may be with hemianesthesia, is due to a 
lesion in the cms cerebri, provided the two sets of paralysis occur 
simultaneously, otherwise they may be due to two separate lesions. 
(Hughlings Jackson.) 

A very rare condition, of which there are but 27 .cases on 
record according to Darquire, is recurrent paralysis of the oculo- 
motor nerve on one side. The attack begins with violent pain on 
one side of the head, nausea, and vomiting, and these symptoms 
are followed by ptosis, external strabismus, mydriasis, paralysis of 
accommodation, and crossed diplopia. It is seen most frequently 
in women, but may date from as early a period of life as eleven 
months. The attacks may last for a few weeks, and recur often or 
only after a lapse of many years. 

As already stated, a form of alternate ptosis sometimes also 
develops in syphilitic persons. 

Bilateral Facial Paralysis. — Bilateral facial paralysis is a rare con- 
dition, and when it occurs can only be due to a bilateral lesion in 
the cerebrum, to acute bulbar paralysis, to progressive bulbar par- 



THE FACE 41 

alysis, to a lesion in the pons just where the facial fibres decussate, to 
bilateral disease of the pons owing to disease of the basilar artery, 
syphilis at the base of the brain producing a tumor cr inflammatory 
thickening, very rarely to bilateral inflammation of the stylomastoid 
foramina, resulting from cold or double otitis, from toxic multiple 
neuritis, but not from that toxic neuritis due to alcohol. Very rarely 
bilateral facial paralysis results from multiple neuritis in its diph- 
theritic form. 

The development of bilateral facial paralysis due to a double 
cerebral cortical lesion never occurs without evidences of paralysis 
elsewhere in the body, such as monoplegia or hemiplegia. 

The bilateral paralysis of the facial nerve in acute bulbar par- 
alysis is characterized by the limitation of the paralysis, as a rule, 
to the neighborhood of the lips, by dysphagia, lingual paralysis, 
affected speech, paralysis of the ocular muscles, and a rapid pulse. 
This disease is very rare, and depends for its existence upon an 
acute inflammation or myelitis of the medulla oblongata. 

When due to progressive bulbar paralysis (glossolabiopharyngeal 
paralysis) the paralysis is confined chiefly to the lips, and is asso- 
ciated with alterations in the tongue (see chapter on the Tongue) 
and speech, with tremor of the tongue and stiffness of the lips. The 
mouth stands half-open, the lower lip is pendulous, and the patient's 
expression is that of a person about to burst into tears. The symp- 
toms of glossolabiopharyngeal paralysis may, however, be exactly 
reproduced by diphtheritic paralysis, with this difference in prog- 
nosis: the first type always die and the second type often get well. 

In making a diagnosis of bulbar paralysis it should be remem- 
bered that another condition exists in rare instances in which no 
definite pathological changes can be found in the nuclei in the 
medulla oblongata, and yet many of the symptoms manifested 
by the patient are identical with those of glossolabiopharyngeal 
paralysis (true bulbar paralysis). This condition has been called 
" asthenic bulbar paralysis ," and in it we find, as early symptoms, 
that the muscles of swallowing and of speech become easily tired 
on exertion, showing failure of the nuclei of the fifth nerve; that 
defects in articulation and speech are developed, indicating disorder 
of the nuclei of the ninth and tenth nerves; and clumsy movements 
of the tongue are present, which is a sign that the nuclei of the 
hypoglossal and twelfth pair are involved. These symptoms are 
practically identical with those of true bulbar paralysis. What are 
the symptoms which by their presence in the true disease and their 
absence in asthenic bulbar paralysis aid us in separating the two 
affections? The answer to this question is that the drooling of 
saliva, the atrophy of the tongue, lips, and extremities, the fibrillary 
twitching of the affected muscles, and the loss of electrical irri- 
tability in these muscles, all of which symptoms belong to true 



42 THE FACE AND HEAD 

degenerative bulbar paralysis, are not to be found in the so-called 
asthenic form. There is, however, in the latter disease a condition 
rarely found in the degenerative form, namely, paralysis of the 
oculomotor, the lower facial, and the inferior division of the fifth 
or trifacial nerve, causing dilated pupils, diplopia (which, however, 
is not accompanied by strabismus), and ptosis (from the oculomotor 
failure), facial paralysis about the mouth (from facial nerve failure), 
and loss of expression about the eyebrows and forehead (due to 
facial and trifacial failure). Whether the diagnosis be true de- 
generative bulbar paralysis or the asthenic form just discussed, in 
both the prognosis is most unfavorable. Indeed, the asthenic 
form is often the more rapidly fatal of the two. In the latter the 
nuclei in the pons are probably always involved, but, as already 
stated, no pathological changes have been demonstrated in any of 
these nervous centres. 

A very rare affection is oculofacial paralysis, which is congenital 
or develops in childhood, and is chronic. There are present par- 
alysis of the facial muscles and ptosis. 

Facial Spasm. — Spasm of the facial muscles may result from 
functional and organic disease, and occurs far more frequently in 
women than in men. The cause of the functional forms we do not 
understand, but they occur in neuropathic persons and about the 
climacteric period. Rarely the spasm arises from reflex irritation 
through the trifacial nerve, resulting from a decayed tooth or a 
cause in the eye or in the skin. Habit spasm arises from an acquired 
trick. The organic causes are many. Thus there may be an irri- 
tative lesion of the facial nerve trunk or one in the cortical centre 
for the face, a tumor pressing on the nerve at its point of origin, or 
an aneurysm of the vertebral artery. The spasm may be confined 
to one side or distributed over both sides, and may be clonic or 
tonic in type. Sometimes it occurs only on attempted movement; 
in other cases it is constant. The clonic form is the more common. 

Spasm of the face is seen in chorea, convulsive tic, blepharofacial 
spasm, in tetanus, meningitis, and epilepsy. When due to chorea 
it nearly always is clonic or twitching, as it is also in convulsive 
tic and habit spasm, but in tetanus, meningitis, and epilepsy it is 
generally rigid or tonic. In chorea the spasm is most marked about 
the corner of the mouth and the eyebrow or eyelids. The move- 
ments of convulsive tic are exceedingly sudden, darting across the 
face and involving all the muscles supplied by the facial nerve. As 
a rule this affection is unilateral. These spasmodic movements of 
convulsive tic may be almost constant or appear in paroxysms, and 
rarely the muscles of the jaw, the neck, and tongue are affected. 
The disease depends upon a disorder of the facial nerve, or its 
centres, which is not understood. The prognosis is bad so far as 
cure is concerned. Spasm of the levator palpebral superioris muscle 



THE FACE 43 

is sometimes seen as a symptom of exophthalmic goitre. It is called 
"Abadie's sign." 

In blepharofacial spasm there are paroxysmal spastic contrac- 
tions of the orbicularis palpebrarum and other facial muscles. The 
spasm often tightly closes the lids. Generally in children there is 
also photophobia with the spasm of the eyelids, which is often tonic 
in character and generally bilateral. This condition has associated 
with it what have been called "Graefe's spots," 1 namely, the pres- 
ence of spots near the supra-orbital foramen or over the vertebrae, 
which when pressed on cause sudden relaxation of the spasm. These 
should always be sought for, as they aid in giving relief to the 
patient. 

Spasmodic movements about the eyes such as have just been 
described are sometimes paralleled by what is called nictitating or 
clonic spasm, which is probably due to some undiscovered cause of 
reflex irritation. 

The development of facial spasmodic twitching accompanied by 
a sudden burst of explosive speech, repeating the last wcrd heard 
or said by the patient in conversation (called echolalia), or the 
sudden bursting out with some blasphemous cr filthy word (called 
coprolalia), is sometimes seen in neurotic adults or children, and 
is often associated with perversion of mora] sense. It is called by 
Gilles de la Tourette " Maladies des tic convulsifs," but this is an 
unfortunate term, because it is apt to be confused with ordinary 
convulsive tic of children or adults. (See Electric Chorea and 
Myoclonus Multiplex in the chapter on the Hands and Arms.) 

In tetanus the muscles of the jaw, the masseters and temporals, 
are first involved in the tonic contractions, and these are followed 
by rigidity of the muscles of the neck and body. Often the risus 
sardonicus is marked from the first, and the face soon looks like 
that of an old man owing to the muscular contractions. 

In meningitis the characteristic symptoms which label the malady 
render facial spasm a comparatively unimportant symptom, and in 
epilepsy the convulsive seizure soon makes easy the diagnosis of 
the cause of the facial spasm unless the epilepsy is limited in its 
character, when the history of the presence of an aura, or of uncon- 
sciousness, or biting of the tongue may be discovered. 

Spasm or contractions of the muscles of the face sometimes fol- 
low facial paralysis as recovery begins, and the contractures involve 
the formerly paralyzed muscles, whereas in paralysis in the limbs 
the contractures generally take place in the muscles which are not 
paralyzed. Sometimes these contractures in the face are perma- 

_ * This term should not be confused with the more common term ''Graefe's 
sign," used to indicate the condition in exophthalmic goitre, in which the lids 
fail to follow the eyeballs when the patient looks down. 



44 THE FACE AND HEAD 

nent, and are due to incomplete restoration of the functions of 
the muscles affected. 

Care should be taken to remember that not very uncommonly 
contractures in the muscles of the face result from hysteria, and 
that they are often on the side opposite the facial paralysis if the 
latter exists. 

Active spasm of the muscles of the face may follow exposure to 
cold, and it sometimes follows the paralysis due to this cause, or, in 
other words, is a sequence of Bell's palsy. 

THE HEAD AND NECK. 

The Head. — In examining the head we look for variations from the 
normal in its shape, its fontanelles if the patient is a young child, 
the position in which it is held, and its movements as governed by 
the cervical muscles. Of the last I shall speak first, although they 
will be mentioned under the heading of Wry-neck. The head is 
moved abnormally in nodding spasm, in chorea, and in tetanus and 
strychnine poisoning. It is also thrown backward and forward or 
from side to side in epilepsy, and in hysteria or in the convulsive 
seizures occurring in young children. 

Nodding spasm of the head, depending upon somewhat rhythmical 
contractions of the sternomastoid and trapezius muscles, is some- 
times seen in half -fed or rickety children. It also occurs in hysterical 
women, and in men who are not hysterical. The nodding may be 
slow and infrequent, only coming on with excitement, or it may be 
practically constant. It always becomes worse when the patient is 
examined, and may be so rapid and forcible as to seem almost 
severe enough to shake the head off the shoulders. Often the 
muscles involved will be found very rigid. 

If the spasmodic movement be not rhythmical, as it usually is in 
nodding spasm, and yet be more or less constant though irregular, 
the cause is probably chorea minor if it is present in a child, or it 
may belong to the irregular movements of adults classed under the 
various forms of tic or choreiform spasm. (See chapters on the 
Hands and Arms and on Convulsions and Spasms.) 

Wry-neck consists in a drawing of the head to one side by spasm 
of the sternomastoid muscle, and at the same time the head may 
be tilted backward or forward according to the accessory muscles 
which may be involved in the spasm. 

Sometimes a tonic spasm of the sternomastoid muscle, produced 
by exposure to cold or due to a distinct nervous lesion, causes 
the head to be drawn down over the shoulder, but rotated to 
the opposite side; the chin is, moreover, directed upward and 
away from the affected side; bilateral spasm of this muscle causes 
fixation of the head. If the cause be exposure, with resulting 
myositis, the history of exposure, combined with that of a sudden 



THE HEAD AND NECK 45 

onset, will permit a correct diagnosis and a favorable prognosis, 
it being remembered, however, if the patient is a female, that 
hysterical spasm may be the cause. If hysteria is the cause, the 
history of the patient, the presence of alteration in her color fields 
and the other signs of hysteria can probably be elicited. (See 
chapters on the Eye and on the Skin.) On the other hand, if the 
contraction has come on gradually, after some injury or in associ- 
ation with some nervous affection elsewhere, it is probable that a 
true nervous lesion underlies the disorder. 

Rarely the trapezius is the only muscle involved, in which case 
the head is drawn backward and toward the diseased side, or, if the 
sternomastoid and trapezius muscles are both involved the head is 
tilted laterally and backward until the patient looks up in the air. 
Pain in the muscles only occurs from fatigue. Bilateral tonic spasm 
affecting the muscles which support the head can be separated 
from that occurring in tetanus by the fact that in tetanus there is 
a general diffusion of the spasm to other muscles, although in that 
form of tetanus called "head or cephalic tetanus" the diagnosis is 
more difficult. 

Cephalic tetanus usually has the following diagnostic pcints: there 
is a history of infection, the character of the onset is sudden, there 
are trismus, difficult swallowing, respiratory disturbance, and facial 
paralysis with rare involvement of the ocular muscles. The spasm 
in cephalic tetanus is also often increased by movement or by the 
attempt to take food. Strychnine poisoning is also to be thought 
of, but the limited character of the convulsion excludes that con- 
dition. Should the muscles be affected by a clonic spasm the 
head is jerked about instead of remaining fixed. 

Retraction of the head in children is an indication in many cases 
of sericus brain disease, and commonly arises from a basal menin- 
gitis. It is to be remembered that some of these cases recover, 
though such a result is rare. Again, we should not forget that caries 
of the cervical vertebrce may cause this position, or that tender and 
enlarged glands in the neck may produce such a result. Sometimes, 
too, it occurs after falls without there being any other indication of 
meningeal irritation. Rarely in neurotic babies retraction of the 
head, as a temporary symptom, accompanies attacks of indigestion. 
Similarly in adults suffering from cerebrospinal fever the head is 
often held in a retracted posture. (See chapter on Headache.) 

The posture of the head may also aid us in diagnosis when no 
spasm of its governing muscles exists. Thus, chronic deafness in 
one ear may cause the patient to hold one side of his head farther 
forward than the other, in order to catch the sounds he seeks with 
the good ear, and pronounced strabismus or scotoma may cause a 
patient to so carry the head as to improve its sight and avoid 
diplopia. 

Persons suffering from great mental depression with a tendency 



46 THE FACE AND HEAD 

to melancholia often sit for hours with the head bowed forward 
with the chin resting on the chest. 

The changes from the normal in the shape of the head are to a 
certain extent considered in that part of this chapter dealing with 
the symmetry and appearance of the face, but there still remains to 
be discussed the changes in the shape of the head as a whole. These 
occur in acromegaly, osteitis deformans, and in hydrocephalus, 
microcephalus, rickets, idiocy, myxedema, and cretinism. 

The head of hydrocephalus is greatly enlarged above the level of 
the ears, and this causes the face, already having a tendency to 
faulty development, to look small and wizened. The eyes seem 
somewhat bulging, the orbital plates are oblique, and the back of 
the head is flattened. Sometimes in true hydrocephalus the 
fontanelle remains pulsating for a long period. Again, in true 
hydrocephalus choked disk is sometimes manifested quite early. 
(See Chvostek's and Trousseau's Signs.) 

In microcephalus, on the other hand, the head is small and often 
narrow. Technically, the term microcephalus is applied to idiots 
whose heads are less than seventeen inches in circumference. 
Nearly always the head of an idiot is abnormally formed. 

The cretinoid head is large, heavy, and massive. 

When a young child has unusually prominent parietal and frontal 
bones, which seem bulging, and there is a general resemblance 
in the shape of the skull to that of hydrocephalus, we suspect the 
presence of rickets. As a rule, the forehead is broad and high, the 
top of the head flat, and the shape of the head more round than in 
the genuine disease. Sometimes in such a child we find, in addition 
to these changes from the norma), spots of thinned bone in the 
occipital and parietal regions. These may be also somewhat soft- 
ened, and this condition, called "craniotabes," is usually a sign of 
rickets which exists in association with infantile syphilis. Rickets 
is seen nearly twice as often in boys as in girls, and there is usually 
to be found deficient development of the bones everywhere, particu- 
larly in the ribs and legs. (For the rachitic rosary, see chapter on 
the Thorax.) 

The condition of the fontanelles in young children is of impor- 
tance in diagnosis. In the healthy child all the fontanelles save 
the anterior fontanelle close during the early weeks after birth, but 
the latter opening does not close entirely until the infant is about 
one year and a half old. During the first few months this fontanelle 
closes very slowly indeed, but after this time has elapsed its edges 
become rapidly approximated. The presence of other fontanelles 
in a child's skull after it is several months old indicates rickets, 
syphilis, hydrocephalus, or some intracranial growth, producing 
pressure on the cranial bones, preventing their approximation. 
Generally, however, these minor fontanelles are not found open but 
closed, and the condition of the anterior fontanelle is the guide in 



THE HEAD AND NECK 



47 



diagnosis. In severe cases of rickets the anterior fontanelle remains 
open until the third or fourth year, and should the rachitic tendency 
be developed early in life the edges of the fontanelle may not only 
fail to be approximated, but may actually recede from each other. 
Sometimes if the edges of the fontanelle are found to be softer than 
usual the diagnosis of rickets can be so confirmed. If syphilis be 
the cause of the deficient bone development, evidences of this disease 
in mucous patches about the mouth and anus may be found or a 
history of heredity adduced; while if the condition be hydrocephalus 
the fontanelle will be markedly bulging. 

If the skin over the fontanelle be found to be bulging temporarily 
to a slight extent, the cause probably lies in some acute disease with 
fever, producing cerebral congestion; whereas, if permanent and if 
the general dimensions of the skull are not increased, an intracra- 
nial growth may be the cause, or a cerebral hemorrhage, a purulent 
meningitis, or some cystic formation may be present, or sometimes 
a thrombosis of a cerebral sinus produces hydrocephalus and bulg- 
ing. In other cases, thrombosis causes sinking-in of the fontanelle. 
This difference in the tension of skin over the fontanelle aids us in 
separating the meningeal symptoms of pneumonia from those of 
true meningitis, for in the true form the scalp is tense and in 
pneumonia it is often retracted. 

Marked sinking-in or collapse of the fontanelle always indicates a 
grave condition arising from some disease which seriously weakens 
the heart and general circulatory system, particularly marasmus and 
cholera infantum. The other symptoms associated with this state 
are usually a sunken appearance of the eyes, slight duskiness of the 
face, a cool skin, and a rapid, feeble pulse. The patient is almost 
comatose, and there may be slight convulsive seizures. Such a 
condition has been called the "hydrocephaloid state," and has 
been confused with symptoms of cerebral effusion arising from 
tuberculous meningitis. 

If there be marked diarrhea present the following table of Symes 
will serve to clear the diagnosis: 



Hydrocephaloid State from Diarrhea. 

Diarrhea. 

No ocular paralysis. 

No rise of temperature. 

No headache. 

No tension or bulging of fontanelle. 

No rigidity and 

No retraction of head. 



Cerebral Effusion (as in Tuberculous 
Meningitis). 

Constipation. 

Ocular paralysis and squint. 

Slight feverishness. 

Headache (if old enough to complain). 

Bulging fontanelle. 

Rigidity and contraction of head in many cases. 



Sometimes in rachitic babies, auscultation of the fontanelle will 
reveal a murmur, hemic in origin. This murmur may, however, 
occasionally be heard when no such disturbance of nutrition exists. 

Excessive sweating of the head, producing a wet pillow, is often 
an indication of rickets when it occurs in a child. 



4 8 



THE FACE AND HEAD 



The Neck. — A swelling in the neck in the median line, or on both 
sides of the median line, anteriorly, is probably due to goitre. If it 
is associated with cardiac palpitation and distress, exophthalmos, 
tremor, nervousness, and depression of spirits, it is called exoph- 
thalmic goitre (Fig. 7). If these symptoms are absent, the con- 
dition is simply one of overgrowth of the thyroid gland. 




Fig. 7.— Exophthalmic goitre. (Meltzer.) 

Aside from swelling of the glands of the neck due to syphilis, 
Hodgkin's disease (see chapter on Fever), struma, and tuberculosis, 
there may be enlargement of the parotid gland on one or both sides, 
just in front of the ears and extending under the angle of the jaw. 
This swelling may be due to the specific inflammation involving 
these glands, known as mumps, or be due to other infections, such 
as typhoid, typhus, and pyemic fever. If the latter be the cause, 
suppuration usually ensues. Rarely enlargement of the parotid 
glands follows trauma or disease of the abdominal viscera or 
pelvic organs. Sometimes the enlargement is chronic after the 
acute inflammation is passed by. 

(For the movements of the head in epilepsy and hysteria, see 
chapter on Convulsions.) 



. CHAPTER II. 
THE HANDS AND ARMS. 

The general appearance of the hands and arms — The shape of the hands in 
disease — Spasm of the fingers — Tremors of the hands— Paralysis of the hands 
and arms. 

Inspection of the Hands. — The appearance of the hand and arm 
often gives us valuable hints in the diagnosis of disease, chiefly by 
reason of variation in their shape, manner of movement, and general 
consistency; but as all these conditions vary widely in normal 
individuals, we can only regard distinct and well-marked alterations 
from the normal type as indicative of a definite disease. We can, 
however, often gather general information as to the patient from 
the hands, particularly as to his occupation; thus we see the smooth, 
soft hand of the professional man or clerk, the horny hand of the 
laborer, the blackened nails and skin of the machinist, or the blue- 
black dottings of the hand of the miner; and Hirt asserts that 
atrophy of the antithenar eminence often occurs in cabinet-makers, 
perhaps from the excessive use of the plane. 

Even when no pathological condition exists we are wont to regard 
the heavy and somewhat thick and clumsy hand as an evidence of 
a phlegmatic temperament, and the thin, wiry, dexterous hand as 
indicative of the nervous temperament. Similarly, we recognize as 
the hand of the strumous that one in which the fingers are slender 
between the joints and the joints themselves thick and clumsy, or, 
again, in persons with tuberculous tendencies, we see a slender, 
delicate hand, easily compressed and somewhat effeminate in type. 
Very commonly, too, in children who have developed heart disease 
in early life the hand becomes square-looking, and the fingers are 
club-shaped through thickening at the tips. A similar clubbing 
also manifests itself in many cases of emphysema and chronic 
phthisis in adults, and unilateral clubbing with incurvation of the 
nails of one hand is sometimes seen in thoracic aneurysm. 

From the appearance of the nails we can often gain important 
information; thus, whenever the color of the blood in the capillaries 
under the nails is dusky we know that deficient pulmonary function 
exists or that the circulation is impaired, it may be from feeble- 
ness or from cold or from an overdose of one of the coal-tar products. 
In anemia the nails are often very pale, and Stephen Mackenzie 
has asserted that if pressure on the tip of the finger completely 
4 



50 THE HANDS AND ARMS 

empties the capillaries under the nails so that the appearance is 
pale the red corpuscles are present in only half the usual number. 

White spots in the nail may be due to injury of the matrix by 
picking at the base of the nail, or be due to acute fevers producing 
trophic changes. 

When the nails are striated and in longitudinal ridges the patient 
is often of the gouty diathesis, while transverse ridges may indicate 
arrest of nail growth through local injury to the matrix or the 
impairment of the general nutrition as the result of a severe surgical 
operation or prolonged illness. Sometimes these marks result 
from a severe attack of gout, and Fothergill tells us that it took 
about seven months for such a mark to grow out of his nails. 
Ordinarily, this mark will be found about half-way up the nail 
three months after the attack. In hemiplegia or acute infantile 
palsy the growth of the nail of the paralyzed part is generally 
arrested, as can be determined by staining it and watching it from 
day to day to see if the stained part gradually moves away from 
the base. When the nails are distorted and thickened the cause 
may be local injury or peripheral neuritis, or any condition of the 
nervous system resulting in decided trophic influences, as in that 
rare condition syringomyelia. 

Hypertrophy of the nails so that they are abnormally elongated 
is usually associated with thickening and the development of great 
fragility. The nail may even be spirally twisted (onychogyropho- 
sis), or, if very wide, may cut into the skin and produce paronychia. 
These conditions may result from skin lesions, such as eczema or 
lichen ruber, at or near the matrix, or be due to syphilis, and Vogl 
asserts that mere thickening may arise from severe fevers. They 
may also be seen in cases of Raynaud's disease, or in sclerodactyle, 
and in cases of pulmonary osteo-arthropathy. 

Atrophy of the nails may apparently arise from causes identical 
with those which produce hypertrophy, and Kaposi has seen the 
nails soft and membrane-like, with abscesses under them, from 
psoriasis of the fingers. 

A diagnostic indication given by the fingers is seen in dactylitis 
due to syphilis. Similar deformity, often multiple, also occurs in 
scrofulosis or tuberculosis. In other cases this is rep]aced by an 
eruption on the skin of the hand characteristic of syphilis. Another 
indication is seen in the ulcers at the bases of the finger nails, with 
ecchymotic spots on the skin, produced by the chloral habit; and 
still another is the sores seen at the bases of the finger nails in 
persons who handle irritating drugs, such as elaterium. (See 
chapter on the Skin.) 

Congested veins on the hand may indicate obstruction to the 
venous circulation of the arm, or general lack of vascular tone and 
a feeble heart. 



INSPECTION OF THE HANDS 5: 

When the hand is cold and clammy the condition may be due to 
bromidrosis, or a local disturbance in innervation of the sweat 
glands. It is often seen in cases of so-called spinal irritation and 
nervous exhaustion. Excessive sweating of the hand is also often 
seen in cases of progressive muscular atrophy. 

There are two sets of movements associated with the muscles of 
the wrist and hand which possess grave prognostic and diagnostic 
importance in the presence of exhausting fevers. The first of these 
is twitching of the muscles of the forearm (subsultus tendinum.) It 
indicates severe and dangerous disease. The second is picking at 
the bedclothes. The grave import of this dangerous symptom, 
" picking up the bedclothes^ or carphologia, was recognized by 
Shakespeare in his description of the death of Falstaff: "After I 
saw him fumble with the sheets, and play with flowers, and smile 
upon his fingers' ends, I knew that there was but one way; for his 
nose was as sharp as a pen." Hippocrates has well emphasized the 
gravity of this symptom, for he says: "In acute fevers, in peri- 
pneumonias, in pleuritis, and in headaches the hands are moved to 
and fro about the face, seeking in the void, as if gathering bits of 
straw, picking at the coverings, or detaching objects from the walls 
of the room, constituting so many signs of a fatal termination." 

The fingers are often distorted and twisted out of their normal 
position from the trophic changes which take place in gout and 
arthritis deformans (rheumatoid arthritis) (Fig. 8). In gout the de- 
formity invades the small joints in particular, and in many instances 
appears most marked in the forefinger. Fixation and deformity of 
the fingers occur through the deposit of urate of sodium in large 
amounts about the joints in their tendons and sheaths, so that the 
fingers are as in splints. The knobs of urate of sodium appear as 
hard, white masses, and, if very superficial, as glistening masses, the 
surfaces of which often break down and allow the escape of material 
looking like powdered wet chalk. The joint surfaces themselves 
are not primarily much altered, but secondarily grave changes 
occur in them. 

Very commonly in gout the only joints of the hand which are 
involved are the first joints of the fingers, a knob developing on 
either side of the knuckle (Fig. 9). The little finger in gout is 
often bent at an acute angle at the middle knuckle, so that it is held 
in an awkward, hooked position. This is most commonly seen in 
women, while in men it is common to see forced flexion of the first 
phalanx of the middle finger into the palm of the hand, even when 
very little if any deposit of urates has taken place. This drawing 
down of the fingers is considered by Paget to be pathognomonic 
of gout, although the patient will claim that it is due to the use of a 
cane, a hammer, or other extraneous cause. 

Distortion of the hand with drawing of the finger or finders into 



52 



THE HANDS AND ARMS 



the palm may be due to Dupuytreti's contraction, which results 
from burns or other injury to the palmar fascia. 

While the history of the patient, the localization of the manifes- 
tations of the disease, and its character render a differential diag- 
nosis between the hand of gout and that of arthritis deformans a 
possibility, it should not be forgotten that the deformities of gout 
may take every position assumed by those of arthritis deformans. 

In arthritis deformans the distortion of the hand may be far more 
marked than in gout, for here there is not a splint-like deposit about 
the joint, but in its stead the development of exostoses on the edges 
of the articular surfaces, which at once lock and disjoint the fingers, 
while at the same time the opposite side of the joint may be par- 
tially absorbed, so that dislocation is still more readily produced. 
As a result there is sometimes developed what is called the "seal-fin 




Fig. 8. — Arthritis deformans in a woman of twenty-one years. Characteristic 
distortion of ring finger on left hand and seal-fin hand on right side. (From 
the author's wards.) 



hand" (also seen in cases of gout), a hand in which the digits are 
deflected chiefly toward the ulna, through the action of the extensor 
muscles, which are supplied with nerves which are renexly irritated 
by the condition of the joints, and thereby cause spasm (Charcot) 
(Fig. 8). 

The term Heberden's nodes is applied by some to the exostoses at 
the sides of the phalangeal joints met with in rheumatoid arthritis 
or arthritis deformans; by others, as by Duckworth, to somewhat 
similar gouty deposits. These are sometimes called "Haygarth's 
nodosities." 

Chronic rheumatism may produce gradual changes in the shape 
of the hand chiefly through disuse and the alterations which it 
causes in the capsules and ligaments. The chief alteration is immo- 
bility or stiffness. Some persons believe that when the hand wastes 



INSPECTION OF THE HANDS 



53 



it does so not from disuse, but through reflex nervous influences. 
Chronic rheumatism rarely, if ever, occurs in the hands alone, but 
when it does the joints are often swollen and somewhat tender, but 
never as hard as in gout. 

The finger-joints are not commonly involved in acute articular 
rheumatism, certainly very rarely as the only manifestation of the 
disease. The inflammatory process is more apt to be about the 
ball of the thumb, or in the wrist and carpal joint. The hand is seen 
under these circumstances as a clumsy, swollen mass, puffy, and 
exquisitely tender and hot. Sometimes it is quite red at the joints, 

Fig. 9 




Heberden's gouty nodes. Illustrat- 
ing common forms of terminal phalan- 
geal deflection. Forefinger and little 
finger of a woman aged seventy years. 
"Crab's-eye" cysts over the joints are 
also depicted. (Duckworth.) 




Nodular swellings (Heberden's 
nodes) due to gouty arthritis on the 
forefinger and little finger of a woman 
fifty years. (Duckworth.) 



but otherwise quite pallid, particularly in the puffy, edematous area 
on the back of the hand. The presence of intense local inflamma- 
tion, the history of sudden onset, and the intense pain on movement 
readily separate acute rheumatism from chronic gout and arthritis 
deformans, and leave it to be separated from sprain, septic arthritis, 
and deep-seated inflammation of the hand proper. The first is 
excluded by the history, the second by the history and general lack 
of evidence of gonorrhea or sepsis or purpura, and the third by the 
lack of accompanying general systemic disturbance and the absence 
of a history of traumatism or infection. In this connection it should 



54 THE HANDS AND ARMS 

not be forgotten that synovitis of the joints of the hands, wrists, 
and elbows sometimes occurs during the fall of temperature in 
scarlet fever, and is often not associated with any rise of temperature 
as a result of its development. The condition is sudden in onset 
and usually rapid in its course. The same state may exist in the 
joints of the lower limbs, but Marsden found it in the hands and 
wrists in 72 instances out of 100 cases, and only 25 times in the 
large joints out of 100 cases. The condition usually appears, how- 
ever, in rheumatic children and those with a rheumatic heredity, 
and is generally relieved by salicylates, so it is not a pure septic 
arthritis. 

The nervous disturbances which change the appearance of the 
hands are very numerous. 

Angioneurotic edema is not peculiar to the hand, although fre- 
quently involving this part of the body. It consists of a swelling 
varying in size from a dime to a silver dollar, which is not edema- 
tous in the sense that it can be pitted on pressure. This swelling, 
which may be multiple, red in cclor, or pale and waxy in appear- 
ance, lasts but a few hours or days, disappears, and often speedily 
returns. 

Somewhat allied to angioneurotic edema is that condition of the 
hand (or toes) characterized by a white and waxy or slate color of 
the ringers, associated with coldness, swelling, and mottling of the 
skin, termed Raynaud's disease. Often this is a passing condition, 
but in its severe forms there is finally developed dry gangrene 
in the fingers involved. The conditions of the hand resembling it, 
from which it must be separated, are senile gangrene, in which the 
advanced age of the patient and the presence of diseased and thick- 
ened bloodvessels will enable us to decide on the latter as the cause; 
frost-bite, in which the history of exposure will be of value, although 
exposure to cold often precipitates an attack of Raynaud's disease; 
ergotism, which can be discovered by the history of the patient 
having for a long time taken food which may have contained bad 
rye; leprosy, which will probably be seen more marked in other 
parts, and in the patches of which can be found the leprous bacillus ; 
and alcoholic neuritis, of which I shall speak later. (See chapter 
on the Skin.) 

In that state known as Morvan's disease, or " painful anesthesia 
with whitlow," there is a slowly progressive loss of power in the 
hand, with atrophy and ulcers about the bases of the nails. Some- 
times the terminal phalanges undergo necrosis, and enlargement 
of the fingers, through swelling, may be very marked. It is prob- 
able that this condition represents two separate lesions, namely, 
neuritis and syringomyelia, and it is an exceedingly rare disease. 

Swelling of the hand, followed in some months by rupture of the 
skin, may, in a person from the tropics, mean mycetoma, which is, 



INSPECTION OF THE HANDS 55 

however, seen more commonly in the lower extremity as " Madura 
foot." 

In addition to these trophic changes in the hand we have the 
so-called "spade-like" hand seen in myxedema, acromegaly, and the 
pulmonary osteo-arthropathy of Marie. In myxedema the deform- 
ity depends upon the alterations in the subcutaneous tissues, rather 
than on changes in the bones, so that the hand is swollen or boggy 
looking, but does not pit on pressure as in true edema. In acro- 
megaly the enlargement is chiefly osseous, as it is also in pulmonary 
osteo-arthropathy, the formation being on a gigantic scale. In the 
latter disease, however, the hands and feet are alone affected, and 
the enlargement is not symmetrical. Further, this condition is 
nearly always associated with changes in the lungs, such as emphy- 
sema, tumors, and old bronchial troubles. The hands are not only 
greatly enlarged, but deformed, so that a side view of the finger tips 
reminds one of the shape of a parrot's beak, the nail being turned 
over the end of the finger. This is particularly well-marked in the 
thumb. 

The differentiation of pulmonary osteo-arthropathy from acro- 
megaly is to be found in the fact that in the first-named disease there 
are no changes in the face, the skin, lips, or orbital ridges. Neither 
is there spinal kyphosis in the cervical region, although it may be 
present lower down. Again, in pulmonary osteo-arthropathy the 
long bones of the upper extremities are greatly enlarged in their 
epiphyses, while in acromegaly they are not so locally enlarged. 

Alterations in the contour of the hand are, however, far more 
frequently produced by atrophic processes than by those which 
result in hypertrophy. They arise in cases of paralysis not only 
from wasting of the muscular tissues, so that hollows or sunken 
places occur, but also from the distortions caused by the con- 
tractions cf healthy muscles, which, having no opposition as in 
health, speedily draw the bones of the hand into abnormal positions. 
In other cases the diseased muscular fibres may be spasmodically 
contracted, overcoming the resistance of the healthy muscles. 

The wasting of the hand seen in old age, particularly in women, 
and in advanced phthisis, diabetes mellitus, and other conditions in 
which the tissues of the body in general lose their plumpness, is so 
universally distributed that a diagnosis of the cause is not difficult. 
On the other hand the wasting due to nervous lesions is generally 
not universal, but limited to a single muscle or group of muscles, 
the remaining portion of the hand having its normal appearance 
or being only indirectly influenced. 

Under the name of "claw-hand" or u main-en- griff e" we find 
a deformity of the hand which is in itself very characteristic, 
although indicative of several causes which all operate in an 
identical manner. The back of the hand loses its normal convexity 



56 THE HANDS AND ARMS 

and becomes somewhat concave, the tendons on the extensor 
surface stand out in ridges, the proximal phalanges are drawn back- 
ward toward the wrist, while the second and third phalanges are 
drawn toward the palm of the hand (Fig. 10). Sometimes, how- 
ever, the tips of the fingers are drawn toward the back of the hand. 
This deformity results from atrophy and paralysis of the interossei 
muscles and lumbricales, which are supplied by the median and 
ulnar nerves. The extensor communis digitorum and flexor digi- 
torum produce a dorsal flexion of the first phalanges and a complete 
palmar flexion of the second and third phalanges. A certain amount 
of immobility is also caused by the fact that flexion of the hand is 
impossible in the fingers and almost lost at the wrist. 






Fig. io. — Claw-hand. (Gray.) 

The claw-hand having been recognized, it remains to be decided 
what are its causes. It may be due to disease of the peripheral 
nerves (the ulnar and median) , of the cells in the spinal cord, and 
of the cells in the cerebral cortex in the hand area. 

Taking up for consideration paralysis of the median and ulnar 
nerves as a cause of claw-hand, we find that the most common cause 
is a neuritis produced by some mechanical injury resulting from 
an accident, or from the following of some occupation in which, for 
example, the artisan presses his elbow constantly on some hard sur- 
face. The deformity may be, therefore, either unilateral or bilateral 
(generally the former), and there will be evidences of local injury, 
or a history which will indicate that the lesion is peripheral. Further 
than this, there will nearly always be found, in ulnar and median 
injury, sensory as well as motor paralysis; and Hirt asserts the 
remarkable fact that the claw-hand may develop in cases in which 
sensory disturbances are the only evidence of median and ulnar 
difficulty — in other words, before motility is lost through paralysis. 
(See chapter on the Skin, Anesthesia of the Skin.) Toxic neuritis 
very rarely, if ever, causes claw-hand, as the musculospiral nerve is 
more commonly affected in this condition and the extensors become 
paralyzed. 



INSPECTION OF THE HANDS 



57 



There are several spinal causes of claw-hand, the most important 
of them being progressive muscular atrophy or chronic poliomyelitis, 
that disease in which there are atrophy and abnormal change in 
the anterior horns of the gray matter of the spinal cord, particu- 
larly in the cervical region (Fig. n). It will be remembered, too, 
that the anterior nerve roots and motor nerves become involved in 
this process. As a result of these changes, we have developed loss 
of power in the hand and arm followed by the development of a 
claw-hand from wasting of the same muscles, as already described, 
the disease process being generally bilateral, though beginning 




Fig. ii. — Areas of spinal cord involved in progressive muscular atrophy. The 
areas involved are the anterior horns of gray matter chiefly (shading heavy) 
(i) and the anterior lateral tracts (2) and anterior root zones. The anterior 
nerve roots which arise from the anterior horns also atrophy, and the atrophy 
extends all the way to the nerve plates in the muscles — along the nerves. 

unilaterally. As progressive muscular atrophy often makes its 
first manifestation in these muscles, the hand affords much 
diagnostic information in suspected cases, and if the patient with 
this disease be watched as he unbuttons his coat, it will be found 
that he does not use his thumb and first finger, but pushes the 
buttons or the edge of the buttonholes with the back of his fingers. 
The additional symptoms are slight, aching or paresthesia in the 
affected parts, and the spread of the paralysis, as its name 
indicates, from muscle to muscle (Fig. 12). Thus, beginning 
in the ball of the thumb it passes to the interossei and thence up 



58 



THE HANDS AND ARMS 



the forearm and arm. Sometimes, however, the forearm muscles 
escape, and the shoulder muscles are attacked secondarily. Very 
rarely are the shoulder muscles first affected. Soon after this the 
dorsal muscles fail and lordosis begins, or the head falls forward on 
the chest. Finally, the respiratory muscles are attacked. Fibril- 
lary tremors are generally observed in the affected muscles. No 
vasomotor change, sensory loss, nor pain occurs in the affected part, 
but, finally, the reactions of degeneration develop. The disease 
may last for many years. 




Fig. 12. — Hand and forearm in chronic spinal muscular atrophy, showing 
especially wasting of thenar and hypothenar eminences. (Dercum.) 



As the result of the acute poliomyelitis of infancy, we may also 
have the hand distorted by contractures, such as forced exten- 
sion in paralysis of the flexors, forced flexion in the paralysis of the 
extensors, and claw-hand in paralysis of the interossei. In pro- 
gressive muscular atrophy the atrophy often precedes the par- 
alysis, whereas in poliomyelitis the paralysis preceded the atrophy, 
so that in the former the reaction of degeneration develops late, and 
in the latter develops early. 

A somewhat claw-shaped hand is also sometimes seen in that very 
rare condition called Morvan's disease, but it has not the character- 
istic appearance of main- en- gr iff 'e, there being a slow symmetrical 
wasting of the muscles with a drawing of the ringers into flexion. 
There are also analgesia and painless whitlows. It usually occurs 
in young and middle-aged males. Morvan's disease results from a 
gliosis of the spinal cord combined with a peripheral neuritis. 

Another spinal lesion producing great alterations in the appear- 
ance of the hand and arm, through wasting of the thenar and anti- 
thenar and interossei and the muscles of the arm, is amyotrophic 
lateral sclerosis. Here again the hand often shows the first mani- 
festations of the disease in the loss of power of which the patient 
complains. The early symptoms of amyotrophic lateral sclerosis 
may closely resemble those of progressive muscular atrophy in the 
loss of power in the thumb muscles, but in this disease the reflexes 



INSPECTION OF THE HANDS 



59 




are markedly increased in the affected muscles, whereas in progres- 
sive muscular atrophy they are lost, although fibrillary muscular 
twitchings may be caused by tapping. Again, the patient is usually 
manifesting some of the symptoms of lateral sclerosis when he 
comes before the physician, such as weariness, stiffness, and loss of 
power in the legs. (See chapter on the Legs, Paraplegia.) There 
are also exaggerated knee-jerks, ankle-clonus, and Babinski's sign; 
wrist- jerk is marked. 

Wasting of the muscles of the hand, causing distortion, may 
also be due to syringomyelia, but there will be, with this loss of 
power, a dissociation of sensation, 
pain and temperature sense being 
lost while tactile sensation is pre- 
served. Often in syringomyelia there 
will be developed an arthropathy of 
the arms such as is seen in the legs 
in tabes. 

Wasting of the hand, with flexion 
and rigidity and sometimes contrac- 
tures, is seen rarely in advanced par- 
alysis agitans in place of the charac- 
teristic tremor. 

In the " cerebral palsy of children" 
sometimes called "spastic infantile 
hemiplegia," the hand may be flexed 
on the forearm, and the forearm on 
the arm, the thumb drawn into the 
palm of the hand and the fingers 
flexed as in Fig. 13. These deformities 
are not necessarily confined to one 
arm alone, but are sometimes bilat- 
eral. A peculiarity of these cases is 
that the muscles waste very slightly, 
and do not develop the reactions of 
degeneration, so that the case separ- 
ates itself from poliomyelitis. The 

fingers in the cerebral palsy of children can often be placed in 
curious positions with ease, and, if the limb be suddenly flexed, a 
lock-like sensation will be imparted to the physician's hand. 
Convulsive seizures of an epileptiform type are very frequent 
in these cases. 

Again, in persons who have had apoplexy it is not uncommon as 
times goes on for the temporary spasm seen in the muscles of the 
hand and arm to be replaced by permanent contractions resulting 
in deformity. These contractions, if they occur early, arc an 
evidence of irritation of the pyramidal tract or the fibres just 



Fig. 13. — Right hemiplegia, 
with contractures and retarded 
growth of arm. Onset of disease 
at eight years of age, following 
typhomalarial fever. (Sachs.) 



60 the hands and arms 

behind the knee of the internal capsule, and are of serious import, 
as they indicate the extension of marked inflammatory processes. 
When they come on later they show that a degenerative process is 
descending the pyramidal tracts. Wasting finally comes on. (For 
further discussion of the significance of paralysis in the arm and 
hand, see succeeding pages and chapter on Hemiplegia.) 

A very important point always to be remembered in examining 
contractures of the hand and arm, or of the lower limbs, is the fact 
that they often are due to hysteria, in which case the history is that 
they set in suddenly, and they are generally accompanied by other 
hysterical manifestations, which can be discovered if sought for. 
As a rule, the muscles do not waste or develop degenerative reac- 
tions, but rarely such wasting may occur. Care must be taken in 
giving a prognosis for cases of hysterical contracture, since organic 
lesions sometimes supervene. Charcot states that if the con- 
tractures persist when the patient is under anesthesia, and the 
muscles are atrophied, organic disease exists. It is important to 
remember this, for these contractions may be practically per- 
manent when once induced, and, as injuries may produce either a 
true organic or a false hysterical contracture, much medicolegal 
interest centres about this differential diagnosis. 

When in the course of an acute illness in a child the fingers are 
drawn down into the palm of the hand, with the tips touching the 
palm and the thumb turned in beneath them, with its tip press- 
ing the palm, the patient may have meningeal congestion or in- 
flammation, or hydrocephalus, and a general convulsion may be 
imminent. 

When the fingers are bent toward the palm, but the tips extended 
and the thumb turned in ("the accoucheur's hand"), the position 
is typical of tetany, but in this condition the rest of the body will give 
evidence of involvement. The nervous irritability in this condition 
is greatly increased, and pressure on a large bloodvessel or nerve 
trunk will often produce the spasm. Gastric dilatation or disease 
of the parathyroids will often be found with tetany. In other cases 
it appears to be due to profound debility, as after prolonged lactation. 
(See Tetany in chapter on Convulsions and General Spasms.) Care 
must be taken to separate the so-called carpopedal spasm of 
rickety, hydrocephaloid children from true tetany, in which the 
body is usually involved, and from spastic paralysis due to infantile 
cerebral palsy. 

Spastic rigidity of the arms is often one of the earliest signs of 
chronic hydrocephalus, even before the skull begins to enlarge, and 
convulsions may be present from time to time. In congenital 
spastic rigidity due to sclerosis or defective development of the 
cortex cerebri the spastic condition is usually confined to the legs. 
(See chapter on the Legs and Feet). 



INSPECTION OF THE HANDS 6 1 

Spasm of the fingers of a rigid type on attempting to make cer- 
tain movements is also seen as the result of excessive use of the 
part involved, and occurs in seamstresses, cigarette-rollers, cigar- 
rollers, typewriters (rarely), telegraphers, milkers (rarely), persons 
who use a pen to excess, and in piano, flute, clarionet, and violin 
players, or in persons engaged in any occupation requiring constant 
and comparatively minute and well-coordinated effort. It seems 
to be more common in men than in women by a large proportion 
(39 to 4) . Sometimes paralysis, tremor, or vasomotor disturbances 
take the place of occupation spasm. 

The spasm resulting from occupation must be separated from that 
sometimes seen in the hand in posthemiplegic chorea, and that 
due to irritative cerebral foci, such as tumors of the brain. The 
history nearly always clears up the diagnosis. Spasm of the 
muscles of the hand and arm, rhythmical or otherwise, may also 
be due to hysteria, and may resemble when due to this cause, true 
tetany (not tetanus). 

The position of the hand may be very various. Thus, the hand 
may drop edgewise from the radius toward the ulna in cases of 
rheumatoid arthritis, from paralysis of the extensors on the radial 
side of the forearm, resulting from neuritis or acute infantile polio- 
myelitis, while marked wrist-drop may occur from paralysis of 
the extensors in chronic lead poisoning, or in any form of neuritis, 
toxic or otherwise, involving the nerve supply of these muscles 
(musculospiral nerve). Wrist-drop may also be developed by 
pressure upon the musculospiral nerve, as in crutch palsy. If the 
wrist-drop is bilateral, it may be due to toxic neuritis; but if uni- 
lateral, it is probably, but not positively, due to pressure paralysis 
from sleeping with the head resting on that arm, or from pressure 
by a crutch, or from some similar pressure capable of injuring the 
nerve. Very rarely unilateral wrist-drop is seen in lead poisoning. 
When lead is the cause, the supinator longus usually escapes, as 
does also the short extensor of the thumb, so that the forearm can 
be flexed and the thumb extended. Pain is rarely present in pres- 
sure or lead wrist-drop, but is present in wrist-drop due to alcoholic 
and other forms of toxic neuritis. Often, too, in these cases the 
flexors are considerably involved. (See part of this chapter on 
Brachia] Monoplegia. 

Choreic movements of the hands and arms in children are seen 
chiefly as a manifestation of chorea minor. They are usually met 
with in rheumatic and neurotic children, and heart murmurs are 
common. These cases are apt to be irritable and frequently 
present considerable mental hebetude. The first evidences of spasm 
may be developed in the hand, and be limited to that member in 
rare cases, and the hand often drops things that are placed in it. 
The hand itself is rarely involved alone, and the muscles of the arm 



02 THE HANDS AND ARMS 

toss the entire arm and hand with a fidgety, jerking movement 
which is very characteristic. A form of chorea minor, usually 
limited to the arm, is called paralytic chorea. It comes on suddenly, 
and is characterized by loss of power with a few feeble twitches. 
It affects only children. The same term, "paralytic chorea," is 
also applied to a condition sometimes seen after an apoplectic 
stroke, choreic movements taking place as degenerative changes in 
the muscles are developed. Sometimes choreic movements come 
on in the latter half of life, often preceded by emotional disturb- 
ances. These movements are not true chorea. They are often 
called senile chorea. 

In some cases of adult chorea the patient tends to become 
maniacal, particularly toward night. Such cases usually occur 
in women, and the prognosis as to life is bad. 

Several other affections which somewhat resemble true chorea are 
sometimes met with, but all of them lack, with one exception, the 
peculiarity of its movements. One of these is what has been called 
habit chorea, or, more correctly, habit spasm, in which condition 
the patient acquires a nervous trick of jerking a muscle or a set of 
muscles. Unlike true chorea, it is more frequently seen in adults 
than children. Its limitation, as a rule, to a single set of muscles 
and the history of the case usually separate it from chorea minor, 
and it is to be recalled that the movements consist in sudden twitch- 
ings rather than jerking, irregular muscular movements. 

In paramyoclonus multiplex the disease, as the name implies, 
usually involves symmetrical parts, the contractions of the muscles 
appear in paroxysms, and the muscles involved are usually the 
biceps, deltoid, and triceps in the arms, and the quadriceps femoris 
and calf muscles of the lower limbs. Myoclonus multiplex is a 
disease of adult life, and chorea is usually seen in childhood. Some- 
times the muscles in myoclonus are exceedingly irritable. 

Under the name of electric chorea, or "Dubini's disease," Dubini 
described a disease, affecting both sexes and all ages, in which sud- 
den shock-like contractions of the muscles take place, as if they 
were being stimulated by a slowly interrupted faradic current. 
The disease usually begins in the upper extremities, and gradually 
involves the rest of the body, and progressively passes to a fatal 
issue. This is a very rare disease, and the sudden contraction of 
the muscles in tonic spasm separates it from chorea. 

Still another form of electric chorea is that of Bergeron, which is 
probably identical with what has been called hysterical chorea. 
Here, again, the shock-like muscular contractions are manifested 
chiefly about the shoulders. The patient is usually a female, and 
has the stigmata, sensory and otherwise, of hysteria. (See chapters 
on the Skin, Eye, and Feet and Legs.) 

Again, the physician may meet, exceedingly rarely (almost never 



TREMORS OF THE HAND AND ARM 63 

in the United States or England), with a condition called convul- 
sive tic or palmus, which has also been called "the jumpers," in 
which the movements are not in the slightest degree like true 
chorea, but are sudden muscular movements, usually imitative of 
the act of some other person or animal. This is often associated 
with echolaha — that is, repeated or echoed speech or coprolalia 
or filthy speech. 

Finally, another very rare disease is that known as Huntingdon's 
or hereditary chorea, a condition in which the twitching usually 
begins in the face and extends to the arms and legs. This ailment 
is hereditary, rarely begins before thirty years of age, is accom- 
panied by progressive mental deterioration, and may last ten or 
twenty years. 

Mercurial poisoning producing tremor may cause so coarse a 
movement in advanced cases that the case may be thought choreic. 
(For a description of tremors, see latter part of this chapter.) 

In u Thomsen's disease" the hand is placed in tonic spasm as 
soon as voluntary movement is attempted. Closely resembling 
Thomsen's disease, or myotonia congenita, is what is called para- 
myotonia congenita, which exists in three forms: first, a patient 
suffering from paralysis agitans on attempting to move is seized with 
rigidity of the muscles, which holds him fixed; second, a patient is 
suffering from ataxia and muscular weakness, and is seized with an 
attack of muscular rigidity; and, third, a patient may have the mus- 
cular fixation occurring just as it does in Thomsen's disease, save 
that it is produced by cold or exposure, and not by intention move- 
ment, and may last for hours. (See also Athetosis.) 

Tremors of the Hand and Arm. — The movements of the hand 
should always be carefully watched in cases of suspected nervous 
disease. The most common alteration from the normal will be 
found to be tremor, which may indicate paralysis agitans, dis- 
seminated sclerosis, general paresis, chronic mercurial, plumbic, 
or alcoholic poisoning, hysteria, senility, Graves' disease, and rarely 
brain tumor. Sometimes a tremor may be found in naturally 
nervous women who are drinkers of tea to excess. 

In paralysis agitans the whole hand is involved, and generally 
both hands are equally affected. The tremor is passive, rhythmical, 
and fine in character at first, but later may be quite coarse. It is 
a slow tremor of about five vibrations per second, which is more or 
less constant, and worse when attention is called to it, but it is not 
greatly increased, and, perhaps, is even decreased, by a voluntary 
act, such as an attempt to raise a glass of water. Very rarely, 
however, the reverse holds true, and the tremor is increased by 
voluntary effort. The fingers are generally semi-extended and the 
thumb is adducted, so that it constantly rubs the index finger with 
its pulp, as if it were attempting to rub off the skin of that member. 



64 THE HANDS AND ARMS 

Frequently there are pain and aching of the extensor muscles of 
the forearm and wrist from the constant exertion. (See chapter 
on the Feet and Legs, the part on Gait.) 

The tremors of disseminated sclerosis are also slow, but coarse in 
character. They are not constant or passive, but are developed 
upon intentional movement, and have a greater amplitude than 
those of Parkinson's disease (paralysis agitans). Indeed, they may 
be so coarse as to be choreic in type, or even ataxic. Often thread- 
ing a needle will be possible for a person with this disease, because 
it is a short act, while lifting a glass of water will be impossible. 
The symptoms of disseminated sclerosis are well summarized in 
the following table drawn up by Charcot. 

I. Spinal Symptoms : 

f Tremor on voluntary movements of the extremities — "intention 
tremor" (arms and head ; more rarely of legs). 
Positive .... -j Titubation. 

| Paresis (spasmodic) of the extremities. 

[ Contracture, with exaggeration of the reflexes— spastic rigidity. 

t No sensory symptoms, or only very slight disturbance. 
{ Vesical disturbance none or very slight. 

II. Cerebral Symptoms : 

Dysarthria— slowness of speech ; scanning of words. 

Nystagmus — blank expression. 

Attacks of vertigo— spasmodic myosis. 

Transitory amblyopia— white atrophy of the papillae. 

Diplopia— associated paralysis of ocular muscles. 

Mental enfeeblement. 

Apoplectiform and epileptiform attacks. 

Difficulty in deglutition. 

III. Abnormal or Unusual Symptoms : 

Trophic Muscular atrophies (amyotrophies), bedsores, 

f Lightning pains. 

j Romberg symptom. 

Tabetic -i Anaesthetic areas. 

j Vesical and rectal paresis. 

'{ Gastric crises. 

Frequent remission of all the symptoms is characteristic of the malady. 

It is not to be expected that all these symptoms will be found 
in one case. But many of them will occur. Charcot taught that 
tremor involving the head indicated disseminated sclerosis, and 
excluded paralysis agitans; but cases of head tremor in the latter 
disease do occur. (See chapter on the Feet and Legs, part on Gait.) 

The tremor of mercurial, plumbic, and alcoholic poisoning resem- 
bles that of paralysis agitans, save that it is more rapid, reaching 
nine or ten vibrations per second, and in the case of alcoholic tremor 
is decreased by a large drink of liquor, while those due to lead and 
mercury may be relieved in a short time by potassium iodide! 



GENERAL MOVEMENTS OF THE HANDS AND ARMS 65 

Further than this, the tremor of alcoholism is generally worse in 
the morning. 

A point of some importance in plumbic neuritis producing tremor 
and wrist-drop is the fact that painful sensations are rarely present; 
in arsenical neuritis, on the other hand, they are often the most 
prominent symptoms, even preceding the motor disturbance. In 
mercurial neuritis, on the other hand, tremor precedes all evidence 
of loss of power, and, finally, may become so coarse as to resemble 
chorea. 

The tremor of general paresis is also rapid, eight or nine per 
second, and is a very fine tremor, which in some instances may 
be felt only when the arm is extended and the finger rested on the 
hand of the physician. In other words, the tremor of the hand in 
general paresis is generally not a predominant symptom, but is 
elicited when the muscles are put upon a strain. In regard to 
the fineness of the tremor of general paresis, it should be remem- 
bered that it closely resembles that of Basedow's or Graves' 
disease (exophthalmic goitre, eight or nine per second), since the 
tremor of this condition is not only equally fine, but generally un- 
seen except when the arm is extended and tips of the fingers rested 
upon the fingers of the doctor. This tremor has been called the 
" railroad-bridge tremor," because of its fineness and vibratory 
character. The individual fingers do not separately tremble in 
Graves' disease. 

In posthemiplegic tremor the trouble is unilateral; there is a 
history of cerebral disease, and paralysis is present. 

Tremor of a very marked character may be due to hysteria, and 
arises most frequently in those who have been exposed to shocks or 
accidents. The tremors may occur constantly or only with inten- 
tion movements, or be increased in amplitude, but not in rhythm 
on movement. The latter form is known as the "type Rendu/' 
and has a rhythm of seven to nine per second, while the slower 
hysterical tremor may be four or five per second. 

Beyond the state of tremor should be recalled the movements of 
chorea, which may be limited to one arm or hand, and which in their 
milder forms may be confused with the pronounced movements 
produced by effort in disseminated sclerosis. The latter are 
often very arrhythmical, and so the choreic movement the more 
closely resembles them; but those of sclerosis are purposive, while 
those of chorea are not, since the movement contemplated in chorea 
is opposed by a contradictory contraction. 

General Movements of the Hands and Arms. — Aside from the 
movements of tremor, careful notes should be made of the move- 
ments of the hand as a whole, of the coordination of its fingers and 
of the arm governing it. Thus, trembling contractions of the 
extensor tendons (subsultus tendinum) are a sign of grave and 
5 



66 THE HANDS AND ARMS 

advanced forms of typhoid fever, and picking at the bedclothes 
(carphologia) is of still graver import. (See beginning of this 
chapter.) Inability to write, to play musical instruments requiring 
the use of the ringers, or to sew, may indicate the rare form of 
locomotor ataxia involving the upper extremities, so that if the 
patient is asked to close his eyes and feed himself the fork or spoon 
misses his mouth through lack of coordination, although loss of 
power may not be present. 

Sometimes in locomotor ataxia as the disease becomes advanced 
paroxysmal twitching of the fingers, may come on, or involuntary 
movements of the fingers occur in association with voluntary 
movements elsewhere. 

In locomotor and Friedreich's ataxia also the movements of the 
hand are often lacking in coordination. The hand may be advanced 
past the object which the patient desires to grasp, or else falls short 
of it. On endeavoring to pick up an object the ringers are spread 
over it like a widespread claw. Generally these ataxic symptoms 
will be more marked in the other parts of the body and be bilateral, 
but Ormerod has reported an instance in which only one hand (the 
left) was involved. This faulty movement of the hand may, how- 
ever, be due to the fact that the ocular muscles are affected, and the 
" erroneous projection" due to this cause leads the patient to pass 
the hand beyond the object reached for. Overdoses of strychnine 
sometimes cause this symptom of "erroneous projection." 

When fibrillary twitchings of the muscles occur and tapping 
the muscles produces idiopathic muscular contraction, progressive 
muscular atrophy may be present or profound asthenia. 

Sometimes, as the result of infantile cerebral paralysis or from 
lesions developing in later life, the muscles of the hand are affected 
by a slow, constant movement, so that the fingers assume curious, 
constrained, and unusual postures, being moved into extreme or 
forced extension, flexion or pronation, or supination. This con- 
dition is called athetosis, and is separable from chorea in that the 
movements are slower and limited to the fingers and wrists, the 
arm escaping. 

In this connection mention should be made of " mirror writing," 
a curious condition in which the patient writes from right tc left 
instead of left to right. It occurs in some cases of mental feeble- 
ness, hereditary or acquired, and rarely in hysteria. " Mirror 
writing" may also be present in cases of cerebral paralysis 

Paralysis of One Arm, or Brachial Monoplegia. — Absolute loss 
of power in one hand and arm without the necessary development 
of subsequent deformity results from cerebral or peripheral lesions, 
as a rule, being rarely spinal in origin, and is called brachial mono- 
plegia. The causes of this loss of power when its origin is cerebral 
may be various. Thus, the lesion may be cortical or subcortical; 



PARALYSIS OF ONE ARM, OR BRACHIAL MONOPLEGIA 67 

that is, in the surface of the brain or in the internal capsule, or 
between the cortex and the capsule in the corona radiata. As a 
rule, however, monoplegia is cortical in origin, for below the cortex 
the motor fibres run so closely together that only a very small lesion 
can involve one without involving all, and so producing a hemi- 
plegia. These cortical lesions when they do occur are generally, but 
not always, associated with a convulsive seizure in the paralyzed 
limb, and Seguin has called this convulsion the "signal symptom" 
indicating a cortical lesion. Brachial monoplegia not due to 
hysteria or neuritis, preceded and accompanied by a convulsicn and 
loss of consciousness, and lacking in signs of involvement of lower 
nervous centres, is, therefore, cortical, and is generally due to the 
formation of a clot in the hand and arm centre resulting from injury 
or from the ordinary vascular causes of apoplexy. In other cases 
it is due to the growth of some neoplasm, specific or otherwise, 
or to a localized meningitis. 

The probability of the lesion being an embolism or thrombosis is 
decreased by the recollection of the fact that the cortex is so well 
supplied by vessels from the pia mater that paralysis of a centre 
from lack of blood supply from such a cause is rare, unless the 
lesion is subcortical, or, in other words, not deep enough to involve 
fibres from other centres as they approach each other, and yet suffi- 
ciently deep to prevent the tissues from partaking of the nutrient 
blood-supply from the pia mater as just mentioned. Aside from 
the discovery of a condition of the internal organs, such as cardiac 
valvular disease or sepsis, which might cause embolism, the diag- 
nosis between paralysis from hemorrhage and embolism is prac- 
tically impossible, and this is also true of the paralysis due to throm- 
bosis, except that in cases of thrombosis we often find the presence 
of general endarteritis or an infectious disease, and the paralysis of 
thrombosis may be slow and gradual in its onset. If the paralysis 
rapidly spreads, the lesion is probably due to a hemorrhage. 

The history of there having been some sudden cause for an 
increase in arterial tension, as by muscular effort, and the presence 
of atheromatous vessels aid us in deciding as to the probability of 
the lesion being due to a hemorrhage, and the sudden onset, coupled 
with the symptoms named, makes the diagnosis clear in a certain 
proportion of cases. 

Neoplasms or tumors of the brain producing monoplegia are 
gradual in their development, accompanied generally by headache, 
by changes in the optic disks, and sometimes by mental disturbances 
or pressure symptoms. A specific history pointing to the formation 
of a syphilitic tumor is of value in the diagnosis, and in all sus- 
pected cases a Wassermann test should be made. (See chapter on 
Headache.) 

If brachial monoplegia results from a lesion in the internal 



68 THE HANDS AND ARMS 

capsule, the lesion must be very limited, or, in other words, large 
enough only to cut off the hand and arm fibres. Tumors and lesions 
from traumatisms in this area are very rare, and hemorrhages, which 
frequently cause paralysis by affecting this area, are generally pro- 
fuse enough to cause hemiplegia — that is, injury of the motor fibres 
supplying the leg muscles as well. Sometimes, however, a sudden 
inflammatory process is set up in the tissues surrounding a tumor, 
and this may precipitate sudden paralysis. 

In monoplegia due to cortical, subcortical, or capsular causes the 
reactions of degeneration do not occur, because the muscles in the 
paralyzed area are still connected with the trophic centres in the 
cord, and this affords us a valuable point in differential diag- 
nosis. 

Sometimes a suddenly developed monoplegia affecting the arm 
comes on as a manifestation of hysteria, and follows the type of true 
cerebral hemorrhage so closely as to almost defy diagnosis. This 
condition may be accompanied by hysterical edema, the hand 
becoming puffy and swollen. The presence of a neurotic tempera- 
ment and other hysterical signs, coupled with the prompt develop- 
ment of contractures, and the fact that the muscles do not rapidly 
waste, point to the cause of the loss of power in some cases, and this 
is emphasized if the presence of hysterical anesthesia of the skin 
can be discovered. Further, if the hand is affected, Patrick asserts 
that in making an attempt to grasp an object the thumb and fore- 
finger are chiefly used; but if the object is placed suddenly in the 
ulnar part of the hand, the remaining fingers can grasp it easily. 
(See chapter on the Skin for additional hysterical symptoms.) 

Brachial monoplegia is very often the result of injury to the 
brachial plexus or to some of its important branches. The symp- 
toms consist in heaviness or numbness of the arm with more or less 
loss of power. The motions of the arm which are particularly 
affected are usually abduction and elevation, which movements 
depend upon the circumflex nerve. If the power of extending the 
arm is lost, the loss depends upon paralysis of the musculospiral, 
which supplies the triceps; whereas if the power to flex the forearm 
is lost, there is paralysis of the musculocutaneous, which is the 
supply of the brachialis anticus and biceps. If the supinator longus 
is involved, the musculospiral is also affected. 

When brachial monoplegia depends for its existence upon primary 
brachial neuritis there is pain in the wrist and hand at first, or on 
the scapula and in the axilla, thence radiating down the arm. This 
pain is constant and dull, and now and then excruciating, and 
is made worse by movement, even when the loss of power is com- 
paratively slight. Sometimes, on the other hand, when the neuritis 
is septic in origin, it may start in the ulnar nerve and gradually 
extend up to the plexus. In still other cases brachial monoplegia 



PARALYSIS OF ONE ARM, OR BRACHIAL MONOPLEGIA 69 

may depend upon fracture or dislocation of the head of the humerus, 
and in such a case the paralytic symptoms are apt to be very well 
developed. The musculospiral nerve is often paralyzed by fracture 
of the humerus, and. this results in paralysis of the muscles of the 
back of the arm and forearm and back of the hand, and loss of 
sensation in the skin covering these parts. 

In all cases of brachial monoplegia due to peripheral lesions, as in 
severe neuritis, we find that atrophy of the muscles comes on very 
rapidly, owing to the cutting off of the muscles from their trophic 
centres in the spinal cord. 

Sometimes in locomotor ataxia the peripheral nerves seem quite 
as much involved as the spinal cord, and symptoms precisely like 
the paralysis of a toxic* neuritis develop. Thus, Strtimpell has re- 
ported cases of musculospiral paralysis from this cause, and Remak 
and Hirt record cases in which the median nerve has been affected, 
so that not only loss of power but wasting of the muscles has re- 
sulted. This is particularly the case if the muscles are much used 
in daily pursuits. The ulnar nerve may also be affected. Such cases 
are separated from pseudotabes, due to neuritis, by the pupillary 
reflexes and ether pathognomonic ataxic symptoms. (See chapter 
on the Feet and Legs and that on the Eye.) Widespread muscular 
atrophy of the arm sometimes takes place in locomotor ataxia as 
a result of a coincident neuritis. 

There are still to be considered two comparatively rare forms of 
brachial monoplegia of the plexus type, namely, that due to 
pressure of growths in the neck or axilla, and brachial paralysis of 
the upper arm type, sometimes called Erb's paralysis. This latter 
form occurs from paralysis of the fifth and sixth cervical nerves 
or their roots. In adults this commonly results from blows or 
heavy weights striking on the shoulder, and in infants from pulling 
on the neck in difficult labor. As already said, it is an upper arm 
palsy, and is due to the loss of nerve supply to the deltoid, biceps, 
brachialis anticus, and supinator longus and brevis, and the supra- 
and infraspinatus muscles. The adult form is often associated with 
anesthesia, and is persistent. In infants it is often temporary, and 
sensory symptoms are commonly absent. 

When the lower arm is paralyzed as the result of trouble in the 
brachial plexus, the lesion is in the nerves arising from the seventh 
and eighth cervical and first dorsal roots, and the muscles affected 
are the triceps, the flexors of the wrist and fingers, the pronators of 
the hand, the extensors of the fingers, and the muscles of the hand. 
The arm can still be raised by the deltoid and the forearm flexed on 
the arm by the biceps. 

When there is wasting with paralysis of the thenar, hypothenar, 
and interossei muscles, not due to progressive muscular atrophy, 
with anesthesia in the arm and forearm in the part supplied by the 



70 THE HANDS AND ARMS 

ulnar nerve, and in addition myosis on the side of the lesion, with 
sluggish pupil, retraction of the eyeball, and partial closure of the 
lids, there is probably a lesion of the first dorsal root of the brachial 
plexus and the communicating branch of the second dorsal. The 
cause may be neuritis or pressure by a tumor. This form is some- 
times called "Klumpke's paralysis." 

(For a description of the areas involved in the spinal cord, which 
cause loss of power in the arms and legs, see chapter on Feet and 
Legs, part on Paraplegia, and tables of localization in that chapter, 
also plates in chapter on Skin.) 

The presence of bilateral brachial monoplegia should always 
make the physician suspicious of lead poisoning or crutch paralysis. 

Apparent brachial monoplegia, in reality a syphilitic pseudo- 
palsy, has been described particularly by Parrot. A child appar- 
ently perfectly well, and but a few weeks old, suddenly loses the 
power of its arm, so that the member hangs like a flail. No wasting 
takes place, no degenerative reactions occur, but there may be 
some pain and crepitation on moving the arm. The cause of these 
symptoms lies in the fact that there has been a separation of the 
epiphyses from the shafts of the bones, with consequent helpless- 
ness. Sometimes general paralysis of the extremities arises from the 
extension of the disease to other limbs. The prognosis as to life 
is bad. 




Fig. 14. — Dynamometer. 

It yet remains for us to discuss the paralysis of several important 
groups of the muscles of the arm. If the forearm cannot be flexed, 
there is loss of power in the biceps and brachialis anticus, and to 
some extent in the supinator longus; and as the first two muscles 
are supplied by the musculocutaneous, and the third by the mus- 
culospiral, such a failure in flexion shows paralysis of these fibres. 

Paralysis of the extensors of the forearm, wrist, and hand, and 
of extension of the elbow, with wrist-drop in consequence, and 



BRACHIAL PARESTHESIA 



71 



flexion of the tips of the lingers, is due to disease affecting the 
musculospiral nerve, but the fingers can still be partly extended 
through the action of the interossei and lumbricales, provided the 
tips are flexed. The back of the hand and wrist become unduly 
prominent after a short time because of the forced flexion cf the 
hand and rapid wasting of the extensors. In most cases the supi- 
nator longus, which supinates the forearm after it is pronated, is 
paralyzed. When the ability to pronate the forearm is greatly 
impaired, and the thumb is extended and abducted, so that it can- 
not be brought in contact with the tips of the fingers, the trouble 
is probably paralysis of the median nerve, and this is confirmed if 
all the phalanges are paralyzed except the first. 

If the arm cannot be moved outward, away from the body, there 
is paralysis of the deltoid supplied by the circumflex nerve. In 
this connection attention should be called to the loss of power with 
wasting of the muscles seen after direct blows on the muscle or 
after injuries to the joint, sometimes called "joint palsies." 




Fig. 15. — Testing the elbow, or biceps, jerk 



Brachial Paresthesia. — Disturbances of sensation in the hand and 
arm consist in anesthesia, analgesia and numbness, tingling and 
pain. The area of these sensations depends upon the nerve trunks 
involved, and to some extent upon the degree of involvement. 
Thus, if the function of the nerve is merely impaired, the sensation 
may be that of tingling or pain ; if still further impaired, thesensa- 



72 



THE HANDS AND ARMS 



tion may be that of numbness; and if the sensory fibres be totally 
destroyed or paralyzed, absolute anesthesia and analgesia may be 
present. (For methods of testing the various forms of sensibility 
in a limb, see chapter on the Skin.) 




Fig. i 6. — Testing the elbow, or triceps, jerk. 



Physical Methods Employed in Examining the Hand and Arm. 
The Dynamometer. — The use of the dynamometer is to determine 
whether there is a marked difference in the strength of the flexor 
muscles in either forearm. The dynamometer most commonly 
used is that of Mathieu, which is an elliptical spring surrounding a 
semicircular scale over which moves an indicator according to the 
flattening of the ellipse produced by pressure. (See Fig. 14.) 

The Elbow- jerk. — This is produced by striking the tendon of the 
triceps or the biceps, the forearm being somewhat flexed on the 
arm, and supported by an assistant or by the physician himself. 
(See Figs. 15 and 16.) 



CHAPTER III. 
THE FEET AND LEGS. 

The general appearance of the feet and legs when clothed — The gait — Spastic 
paraplegia — Paraplegia without spastic contraction — Crural monoplegia — 
Deformities of the feet and legs — The joints — Alterations in the nutrition 
of the feet and legs aside from a change in the muscles. 

As the physician sees a patient approaching him, he can often 
gain information as to the ailment from which the man is suffering 
by noticing his gait and the appearance of the legs and feet, for, 
while the gait varies greatly in normal individuals, in some diseases 
it is so typical that he who runs may read the diagnosis. A glance 
at the feet revealing one foot more loosely covered than the other, 
or a slit in the shoe, or a very loose lacing, will point to the pres- 
ence of some inflammatory or dropsical swelling, which forces the 
patient to give it room; and if the legs of a man of ordinary build 
look swollen and fill the trousers tightly, while a glance at his face 
reveals that it is puffy, rather than one which is obese, dropsy is 
probably the cause. 

Gait. — Aside from local injuries causing a lame gait, we find that 
gout, rheumatism, and sciatica are the common causes of a limping 
gait, arising from trouble in one leg, and that in such cases there is 
a pained expression of the face at each movement, which shows the 
suffering that walking causes. The gait of such a patient is slow 
and cautious, and he is apt to rest every few steps, bearing his 
weight at such times chiefly on the well leg, or, by mears of his 
hands, upon chairs or tables that may be near. Aside from the 
alterations of gait produced by these causes, we see very typical 
gaits produced by locomotor ataxia, pseudolocomotor ataxia 
(peripheral neuritis) due to alcoholic or lead poisoning, syphilis, or 
peripheral neuritis arising from other causes, hysteria, general 
paresis, chronic myelitis, lateral sclerosis, acute or chronic polio- 
myelitis, pseudomuscular hypertrophy, cerebral infantile palsy, 
multiple sclerosis, paralysis agitans, cerebellar disease, organic and 
hysterical hemiplegia, Friedreich's ataxia, and osteomalacia, and 
the gaits caused by rickets and other bony defects. 

In Locomotor Ataxia the gait is unsteady and waveringly uncer- 
tain, resembling that of a blindfolded person who is told that he is 
approaching some inequality in the floor. The patient continually 



74 THE FEET AND LEGS 

seems to be feeling for the ground with his feet, and carefully picks 
his way along a perfectly smooth surface in a labored fashion, using 
a cane to help him both in the way of support and of feeling the 
ground. Later in the disease the legs may be loosely thrown 
forward in the attempt to walk and joints seem loose and yielding. 
If he looks up from the ground while walking, he sways suddenly 
and may fall; and if prevented from returning his eyes to the 
pavement, almost surely falls if no aid is given him. 

The important symptoms which point to true locomotor ataxia 
are the swaying of the body when the eyes are closed (Romberg's 
symptom), the ]oss of knee-jerk (Westphal's sign), the history of 
gastric, laryngeal, or vesical crises, the presence of numbness in the 
feet, the slow onset of the disease, and the absence of any history of 
exposure to the causes of neuritis. Additional diagnostic points 
are the inability of the patient to stop and turn quickly and steadily 
at the command of the physician. 

Frankel states that in many cases of this disease the sensation of 
passive motion at the joints is impaired. To determine the presence 
of this symptom the toe is grasped by the thumb and forefinger, 
and moved very slowly and gently so as not to disturb the rest of 
the limb. The patient must be blindfolded, and in ataxia fails to 
appreciate the passive joint movement has been made. If all 
these signs are present, and are combined with that important 
symptom, the Argyll-Robertson pupil, the diagnosis is practically 
certain. 

Grube has, however, reported three cases of diabetes mellitus 
producing a pseudotabes due to neuritis which had the Argyll- 
Robertson pupil, and in addition attacks of abdominal pain like 
the crises of true ataxia. 

Another sign of locomotor ataxia is undue relaxation of the mus- 
cles, which has been called hypotonus. This is a point much insisted 
upon by Frankel. He points out that if a healthy man be placed 
in a horizontal position on a couch, he cannot raise the leg very high 
if the knees be kept extended. On the other hand, if he has loco- 
motor ataxia, even with the knee fully extended, he can raise the 
leg to a sharp angle with the plane of the body, amounting to 60 ° 
8o°, or ioo°; whereas in health he cannot raise it to an angle greater 
than 30 to 50 . This is due to the fact that the semimembranosus 
and semitendinosus resist the movement in health; whereas in 
locomotor ataxia they are so relaxed that this resistance does not 
occur. Again, because of hypotonicity of the quadriceps, it may 
be possible in such patients to flex the knees to such an extent that 
the heel can readily touch the buttocks in voluntary motion. So, 
too, the thighs when the legs are flexed may be so widely abducted 
that the knees come in contact with the couch, because of relaxation 
of the abductors. 



GAIT 
The Stages of Tabes Dor.sai.is. 



75 



Initial Period. 


Second Stage. 


Final Station. 


Incoordination, but no change 
of gait. 


Greater inco-ordination, and 
marked ataxic gait. 


Cannot walk because of ataxia. 


Numbness of the feet. 


More marked anaesthesias. 


Extensive anaesthesia. 


Shooting-pains in the legs. 


Pains worse. 


Pains less. 


Diminished or lost knee-jerks, 
one or both. 


Lost knee-jerks. 


Lost knee-jerks. 


Sluggish or lost pupillary reflex 
to light. 


Lost pupillary reflex to light 
and myosis. 


Lost reflex to light, myosis, 
paralysis of accommodation. 


Weakness of sexual function. 


Impotence. 


Impotence. 


Transient diplopia ; transient 
ptosis 


Ocular palsies rare, or marked 
ophthalmoplegia. 


Ophthalmoplegia. 


Sluggish micturition. 


Increased vesical weakness. 


Catheterization needed. 


Optic atrophy. 


Optic atrophy rarely develops. 


Blindness. 


Trophic changes in the joints. 


Trophic changes not so com- 
mou. 


More marked if they began in 
early stage. 


Hemiatrophy of tongue. 


Deafness. 


Increased. 




Laryngeal and visceral crises. 


Not so common. 




Girdle sensation. 


Unnoticed. 



Reflex action is decreased and the gait altered in locomotor 
ataxia, because, though the motor tracts are open, the sensory 
tracts in the nerves, the posterior nerve roots, and the posterior 
columns of the cord are diseased. (See Fig. 17.) For these reasons 
the reflex arc is destroyed and the coordination of the muscles lost. 
The patient cannot tell how to use his muscles unless he can see 
them and coordinate them by the aid of the eye. The sensations 
of formication or numbness are also due to these sensory lesions. 
(For descriptions of motor and sensory tracts of the spinal cord, 
see earlv part of chapter on Hemiplegia and the chapter on the 
Skin.) 

The gait of pseudotabes is sometimes identical with that just, 
described, is usually associated with a history of alcoholic excess, 
and is due to multiple neuritis. In a majority of the cases, how- 
ever, it is distinctive, and has been called the "steppage" gait. 
The foot is thrown forward and the toe is raised so that the heel 
first strikes the ground in much the manner adopted when one 
attempts to step over some obstacle. Sometimes this gait is found 
in cases of arsenical neuritis and that due to lead, but in alcoholic 
tabes there are generally mental symptoms associated with this gait, 
while in lead poisoning the pathognomonic signs of this condition, 
such as the blue line on the gums and wrist-drop, when combined 
with the history, clear up the diagnosis. It must not be forgotten, 
however, that the differential diagnosis of tabes from pseudotabes 



7 6 



THE FEET AND LEGS 



is sometimes very difficult, and as Dana has well said: "When 
Dejerine described as locomotor ataxia a case which now appears to 
have been one of alcoholic peripheral neurotabes, when Buzzard has 
diagnosticated as true spinal tabes a case of postdiphtheria ataxia, 
when Seligmueller mistakes a case of wall-paper poisoning for one 
of true spinal tabes, we may easily suppose that errors have been 
made by many others." Furthermore, it is to be remembered that 
the subject of alcoholic abuse is very prone to be careless while 
"in his cups," as to his sexual relations and so often acquires 
syphilis which in time causes true tabes. 




Fig. 17. — Showing the areas of the cord involved in locomotor ataxia. 1, 
primary lesion in sensory neurones in posterior ganglia; 2, sensory nerve roots 
in which the earliest and most extensive lesions are found; 3, and 4, the shading 
includes both the column of Burdach, the outer, and that of Goll, the inner; 5, 
also Clarke's column in the gray matter. It is to be remembered that the 
lesions of locomotor ataxia are found in the peripheral nerves as well. 

In neuritis causing pseudotabes we have a history of rapid onset 
of the symptoms, paralysis, and wasting of the muscles, an absence 
of vesical symptoms and of the Argyll-Robertson pupils. 

Sometimes not only the gait, but the entire set of the ordinary 
symptoms of locomotor ataxia are aped by hysteria so closely that 
a diagnosis may be almost impossible, but the Argyll-Robertson 
pupil, the lost knee-jerks, and the optic atrophy will not be present 



GENERAL PARESIS 



77 



if hysteria be the cause of the symptoms. On the other hand, 
Romberg's symptom may be marked to an extraordinary degree. 
The patient who is hysterical, in falling nearly always fails the 
same way, keeping her frame stiff like a board. (See chapter on 
Eye for differential ocular symptoms.) 




Fig. i 8. — Showing the spinal areas chiefly involved in Friedreich's ataxia. 
The areas are the column of Burdach (i); the lateral pyramidal tracts (2); the 
columns of Goll (3) ; the posterior nerve roots (4) ; the direct pyramidal tracts 
(5) ; atrophy of cells in anterior horn (6) ; and in the posterior horn (7) ; and the 
anterior jierve roots (8). 



General Paresis. — The feebleness of the limbs, the reflex irido- 
plegia (Argyll-Robertson pupil) , and the ataxic gait sometimes seen 
as the chief manifestations of general paresis may cause an error 
in diagnosis in favor of locomotor ataxia, but careful examination 
will reveal mental feebleness in the paretic case, or at least evi- 
dences of delusions, and if the disease is at all advanced there may 
be a history of the patient having had convulsions or apoplectiform 
attacks. Sometimes there will be found present in paretic dementia 
(general paresis) increased knee-jerks and many of the symptoms of 
ataxic paraplegia, but the associated mental failure and fine in- 
tention tremor of the hands decide the diagnosis in favor of paretic 
dementia. In both tabes and paresis the Wassermann test would 
be positive and the cerebrospinal fluid show an increased lympho- 
cytosis. 



78 THE FEET AND LEGS 

In Friedreich's Ataxia the gait is peculiar. The legs are widely 
separated and moved in an uncertain, hesitating manner, and if the 
feet are placed close together and the patient is told to stand still, 
swaying at once develops. If the eyes be closed, the swaying may 
greatly increase. The movements of the arms are incoordinated. 
These symptoms, which to a certain extent simulate true locomotor 
ataxia, are associated, as a rule, with others which separate the two 
affections, for in this disease the symptoms often come on in very 
early life, there is sometimes nystagmus, usually a history of 
heredity, there is a slow and jerky articulation, scoliosis, and talipes 
equincvarus, but there is no Argyll-Robertson pupil (Fig. 18). 

Furthermcre, Friedreich's ataxia is very rare and locomotor 
ataxia so very common that the former disease can be excluded 
somewhat on this basis. 

The following table shows the differential points between loco- 
motor ataxia and Friedreich's ataxia: 

Locomotor Ataxia. Friedreich's Ataxia. 

Argyll- Robertson pupils. i No Argyll-Robertson pupils. 
No nystagmus. Present late in disease. 

Painful crises. , Crises usually absent. 

Intellect unimpaired. ! Becomes impaired. 
Gait ataxic. Cerebellar ataxic gait. 

Speecb normal. Speech halting. 

No head tremor. Head tremor present. 



Hereditary Cerebellar Ataxia. — Friedreich's ataxia must be 
separated from another very rare disease in which the gait is 
ataxic and the disease hereditary, namely, hereditary cerebellar 
ataxia, in which we have the following symptoms not seen in 
Friedreich's disease, namely, normal or exaggerated knee-jerks, 
Argyll-Robertson pupils, and a beginning of the malady after 
twenty years of age. 

Hereditary cerebellar ataxia may also be confused with dissemi- 
nated sclerosis. 

Disseminated Sclerosis. — The gait in disseminated sclerosis is 
often markedly spastic and paretic — that is, stiff and feeble — and 
may in the early stages of the disease closely resemble that of 
spastic paraplegia due to lateral sclerosis. When the patient 
attempts to pick up a small object with his fingers there are tremor 
and oscillation of the hand. Scanning speech and nystagmus 
develop later on in these cases, and atrophy of the optic 
nerves is a frequent occurrence. It is, however, important to 
remember that multiple cerebrospinal syphilis may closely simulate 
multiple, or disseminated, sclerosis. Sometimes they may be 
differentiated by the fact that in disseminated sclerosis there is 
paresthesia, whereas in syphilis there is more apt to be pain. An 



ATAXIC PARAPLEGIA 



79 



important differential symptom is that nystagmus is rare in syphilis, 
common in disseminated sclerosis, and ocular palsies are common 
in syphilis, rarely so severe in sclerosis, so that complete oculomotor 
palsy with ptosis and squint would be more likely syphilitic than 
sclerotic. (See chapter on the Eye.) 



Hereditary Cerebellar Ataxia. 
1. Gait : ataxic, groggy ; feet wide apart. 



2. Station : Romberg's symptom absent. 

3. Arms: ataxy and some intention tremor. 

4. Oscillations and jerky movements of the 
head and trunk. 

5. Exaggerated contractions of facial mus 
cles during speaking. 

6. Speech: hesitating and abrupt, or simply 
monotonous. 

7. Eyes : jerky nystagmus ; optic atrophy, 
contracted field of vision. The external recti 
muscles may be paretic or paralyzed. 

8. Myotatic irritability increased, knee- 
jerks exaggerated, ankle-clonus ; contractures 
and muscular rigidity. 

9. Mental impairment in varying degrees. 

10. Vertigo sometimes. 

11. Vesical functions rarely affected. 

12. Apoplectiform seizures do not occur. 

13. Heredity common. 



Disseminated Sclerosis. 

1. (a) Spastic paraplegia; feet close together. 
(6) Ataxic, groggy ; feet wide apart, (c) Ataxic 
paraplegia (a +b). 

2. Romberg symptom may be present. 

3. Intention tremor ; sometimes ataxy. 

4. Oscillations and jerky movements of the 
head and trunk. 

5. Twitching in facial muscles during 
speaking. 

6. Laborious, scanning, or monotonous 
speech. 

7. Jerky nystagmus ; optic atrophy, con- 
tracted field of vision ; ocular nerve palsies. 

8. Myotatic irritability increased ; knee- 
jerks exaggerated, ankle-clonus ; contractures 
and muscular rigidity. 

9. Mental impairment in varying degrees. 

10. Vertigo common. 

11. Vesical functions more frequently dis- 
turbed. 

12. Apoplectiform seizures occur in a small 
proportion of cases. 

13. Heredity uncommon. 



Stieglitz has pointed out that in certain cases of acute dissemi- 
nated myelitis and encephalomyelitis following the acute infectious 
diseases, the symptoms of an acute or subacute multiple sclerosis 
are presented, more especially the intention tremor, the increased 
reflexes, and the scanning speech. The disease may intimately 
form the basis of a typical chronic insular sclerosis with its recurrent 
attacks, etc. It may, however — and this is a point of importance- 
subside after a shorter or longer period and end in recovery. 

Myelitis. — In chronic myelitis in the early stages, while motion is 
still preserved, the gait is typically that of feebleness, and the legs 
respond slowly to the cerebral desires, being dragged along after 
the patient, who leans forward, supporting some of his weight on 
crutches or canes. 

Ataxic Paraplegia. — If the lesions of the disease involve the lateral 
pyramidal tracts to a considerable extent, the gait is somewhat 
spastic, and if the sensory fibres are also much involved it may be 
like that of ataxia. Under these circumstances the attitude and 
gait of a patient are sometimes a combination of those of lateral 
spinal sclerosis (spastic paraplegia) and locomotor ataxia. In some 
instances the spastic symptoms are more marked, in others the 



80 THE FEET AND LEGS 

signs of locomotor ataxia are more prominent. This condition is 
called ataxic paraplegia, and in it we find the exaggerated knee- 
jerks of lateral sclerosis associated with the swaying of the body 
(Romberg's symptom) of ataxia. Ankle-clonus and Babinski's sign 
are also present. The crises of locomotor ataxia do not occur, and 
the Argyll-Robertson pupil is usually not present (Fig. 19). 




Fig. 19. — Showing areas of spinal cord involved in ataxia paraplegia, which is 
practically a combination of locomotor ataxia and lateral sclerosis. 1, lateral 
or crossed pyramidal tracts; 2, posterior columns of Goll, and 3, those of 
Burdach; 4, direct pyramidal tracts or Turck's columns. 

Lateral Sclerosis. — In lateral sclerosis the gait is typically 
spastic, the legs being rigid from the hip- joint down, and the toe 
being dragged in a semicircle from behind forward. 

Poliomyelitis. — When the gait of a young child is stumbling, 
or the leg is dragged, or the ankle bends so that locomotion is 
impossible, the probable diagnosis is that the cause is acute polio- 
myelitis. (See Paralysis of the Leg.) 

Pseudomuscular Hypertrophy. — In pseudomuscular hypertrophy 
there is a peculiar waddling gait, a tendency to stumble, the body 
is usually bent forward, and there is difficulty in getting up from 
the floor and on going up and down stairs. The patient in all his 
movements shows a marked loss of power in the legs with a great 
apparent increase in the size of the muscles in the legs. 

The gait of pseudomuscular hypertrophy is sometimes closely 
reproduced in children suffering from severe rickets. The other 
features of the case which may mislead the physician are that the 
child, if fat, will have bulging legs, as if the muscles were hyper- 



PARALYSIS AGITANS 



8l 



trophied, and lordosis due to spinal weakness. In the rickety case, 
however, the knee-jerk is preserved, and in the case of pseudo- 
muscular hypertrophy it is lost. 

Infantile Cerebral Paralysis. — The gait of a child suffering from 
infantile cerebral paralysis is quite characteristic. In the first place 
it is spastic, and the patient walks on the toes, or in some cases 
club-foot develops. The heels are everted and the toes turned 
inward, the knees being so closely approximated that the clothes 
may become worn between them from the rubbing. So great is the 
extension of the feet that the toes are very apt to drag, and, finally, 
the adduction spasm may be so great that the legs overlap each 
other as walking is attempted (Fig. 20). 





Fig. 20. — Spastic paraplegia ; crossed- 
legged progression. (From a patient of 
Dercum's in the Jefferson Medical 
College Hospital.) 



Fig. 21. — Side view of a case of 
paralysis agitans, showing forward 
inclination of trunk. Tendency to 
propulsion. (Dercum.) 



Paralysis Agitans. — In paralysis agitans the patient's gait is 
hurried because, from the bent-over position of the body, the 
centre of gravity is too far forward, and he runs to keep up with it. 

6 



62 THE FEET AND LEGS 

This is called festination. The gait is also somewhat trotting or 
toddling. (See Fig. 21.) 

Cerebellar Disease. — In cerebellar disease the gait may closely 
resemble that of a drunken man, and the patient has the greatest 
difficulty in keeping from sheering off to one side as he walks, 
swaying, too, from side to side (cerebellar titubation). The middle 
lobe of the cerebellum is usually affected; but Nothnagel asserts 
that if these symptoms are associated with paralysis of the oculo- 
motor nerves and other symptoms of brain tumor there is a growth 
in the corpora quadrigemina. 

Hemiplegia. — In hemiplegia the gait is peculiar in the dragging 
along of the paralyzed limb by a peculiar outward swing, which soon 
wears away the sole of the shoe on the inner side near the ball of 
the foot. It is sometimes called a mowing gait, because the leg 
sweeps around in a half -circle. Very often the shoulder opposite 
the paralyzed side is raised in order to tilt the pelvis on the paralyzed 
side, so as to make circumduction easy. 

Hysteria. — The gait of hemiplegia is to be clearly separated from 
that due to hysterical paralysis, for in this condition the leg is 
dragged after the body without the outward swing. It is dragged 
along like the broken hind limb of one of the lower animals, or is 
shoved forward and the well foot drawn after, the reverse of what 
happens in organic paralysis. The footsteps of the hysterical hemi- 
plegic are, moreover, apt to be careful and mincing. Further, the 
loss of power is usually left-sided, and associated with character- 
istic hysterical anesthesia (see chapter on the Skin), and often with 
areas of hyperesthesia. Again, in the gait of hysterical paralysis 
the patient is apt to be excessively laborious in her progress, and 
will exhaust her muscles in her strained movements. An altered 
gait due to irregularly distributed paralysis of groups of muscles 
is nearly always hysterical, and sometimes the patient who has 
hysterical loss of power will suddenly fall through giving way of 
her knees. 

A condition of the gait and station of the patient varying from 
normal, which occurs most commonly in hysteria, consists in -an 
inability to coordinate the movements of the muscles of locomotion 
or those used in standing. This is called "astasia abasia." It is 
in reality a form of ataxia often developing only when the patient 
attempts to walk. There is no loss of power in the legs, but an 
inability to use them regularly or with power while walking, although 
if the patient be made to lie down the movements of the limbs as 
made in walking can be performed perfectly. The knee-jerks are 
not lost, and in addition the general symptoms of hysteria can 
nearly always be found. The body often reels to and fro, and occa- 
sionally the muscles seem to be somewhat spastic. This symptom 
generally follows some severe shock, and is most commonly seen in 
young women. 



PARAPLEGIA 



8,3 



Osteomalacia. — In osteomalacia there is increasing difficulty of 
walking, partly due to pain and partly to muscular weakness. The 
gait is hobbling, tottering, and is made up of short and evidently 
painful steps, "the pelvis and leg being jerked forward as if in 
one piece." The kyphotic deformity of the spine, muscular tender- 
ness, and lateral compression of the chest and pelvis, with dis- 
tortions of the limbs, aid in making the diagnosis. 

Rickets. — The gait of rickets is only peculiar when curvature of 
the limbs or spine destroys the normal posture of the body or 
interferes with the movements of the limbs, and it is nearly always 
more or less waddling. 

PARAPLEGIA. 



Given a case of paraplegia, or paralysis of the lower extremi- 
ties, What may be its cause? It may arise from a cerebral lesion, 
which is very rare, except in children, when it is common, 1 and 
if cerebral it must depend upon a lesion on both sides of the cere- 
bral cortex or in each capsule; that is to say, there must be present 
a lesion in the leg centres on both sides of the cortex or in the fibres 
going to the legs through the internal capsules. 

Much more commonly the lesions causing paraplegia are in the 
spinal cord, very rarely this symptom is due to involvement of the 
nerve trunks on both sides, after they have left the cord, and 
sometimes it is caused by hysteria. When paraplegia occurs in 
a young child it is due in a great majority of the cases to caries 
of the vertebrae, and the pressure so produced does not necessarily 
depend upon compression by the bones, but by the inflammatory 
exudate. 

The spinal lesions giving rise to paraplegia of the lower extremi- 
ties are numerous, and are perhaps best grouped in the following 
table of Bramwell: 



f Inflammation of cord 
Softening " 

Hemorrhage " " 
Tumors " 



1. Organic disease 



Meningitis " " 
Meningeal hemorrhage 
Injuries , 

Tumors 



Medullary. 



Meningeal. 



2 Functional 



Caries of bone 
[ Tumors of bone 

f Hysterical. 

J Reflex. 

I Malarial and ansemi 

[ Dependent on idea. 



Osseous. 



1 Such an occurrence in adults is very rare, but it is quite common in young 
children, as many as 14 per cent, of the cases of infantile cerebral palsy being 
paraplegias. (Sachs.) 



54 THE FEET AND LEGS 

Cerebral Spastic Paraplegia.— The paraplegia of cerebral infantile 
paralysis is spastic, and there is a history of a difficult labor or 
injuries to the head of the child during or after birth. Contractures 
nearly always ensue, and exist chiefly in the adductors of the 
thighs, so that the attitude is very characteristic (Figs. 20 and 22). 
Epileptic convulsions very often complicate these cases. Often these 
paraplegias are not manifested for some months, or even longer 
after birth. In many cases they are first noticed when the child 
attempts to walk and as the lesion does not destroy life it is not 
uncommon to find adults suffering from the disease. 




Fig. 22. — Spastic diplegia, congenital, presenting choreiform and athetoid 
movements. (Dercum.) 

Care must be taken not to confuse the contractures which some- 
times develop as the result of the acute anterior poliomyelitis of 
infancy with the spastic state of the muscles arising from infantile 
cerebral paralysis. These contractions with their resulting deform- 
ity arise in muscles, otherwise healthy, which have been deprived 
of their natural antagonists. These contractures are not spastic, 
often do net occur except upon intention movement and are accom- 
panied by the usual signs of disease of the lower motor neurone. 

Arrested Development— Cerebral spastic paraplegia in infants 
also sometimes comes on in cases of so-called arrested development. 
Such infants present no abnormality for the first few months of 
life, then cease to develop in mental brightness, fail to recognize 
the nurse or mother, cease to play, and gradually present symp- 
toms of bilateral spasticity. There is no history in such cases of 
difficult labor or premature delivery. This condition is sometimes 
called "Little's disease." 

Amaurotic Family Idiocy. — Closely allied to this state is that 
known as " amaurotic family idiocy." In this rare condition, only 
seen so far in the children of Hebrew parents, there is in associa- 
tion with the symptoms just described a pathognomonic ocular 



PARAPLEGIA 



85 



lesion, consisting in the appearance of a whitish-gray patch in the 
region of the macula lutea, which covers an area nearly twice the 
size of the optic disk and causes blindness. In both this and the 
infantile cerebral form of spastic paraplegia the pyramidal tracts 
are degenerated. 

Care should be taken that the spastic paraplegia of rickets is not 
mistaken for a birth palsy. 

Multiple Sclerosis. — A cerebrospinal cause of spastic paraplegia 
in adults is multiple cerebrospinal sclerosis, in which condition 
the loss of power amounts to a paresis rather than the absolute 
paralysis. The presence of intention tremors, exaggerated knee- 
jerks and ankle-clonus, with staccato speech, nystagmus, and 
vertiginous, epileptiform, or apoplectiform seizures, and local 
areas of loss of power elsewhere, associated with the spastic para- 
plegia, renders the diagnosis easy. (See early part of this chapter.) 




Fig. 23. — Shading shows areas involved in lateral sclerosis. 1, the crossed 
pyramidal tracts; 2, the direct pyramidal tract of the cervical region, which is 
affected late in the course of the disease. 



Spinal Spastic Paraplegia. — Lateral Sclerosis. — In the adult, 
when there is loss of power in the lower limbs with spastic con- 
traction of the muscles when the patient attempts to move them, 
so that they become rigid, or if before the stage of rigidity develops 
the gait is spastic and stiff and the reflexes are greatly exaggerated, 
the disease is generally lateral spinal sclerosis (Fig. 23). There is 
also in lateral spinal sclerosis absence of both sensory disorders 
and rectal and bladder troubles, but sometimes there are present 
excessive hasty urination and defecation. 



86 THE FEET AND LEGS 

Strumpell recognizes a rare hereditary form of spastic paraplegia 
appearing early in life and occurring in several members of the 
same family. 

In amyotrophic lateral sclerosis similar symptoms associated with 
wasting of the muscles are present in the later stages, but in the 
early stages the arms are chiefly affected by the wasting and 
paralysis (Fig. 24). (See chapter on the Hands and Arms.) 




Fig. 24. — Showing areas of spinal cord involved in amyotrophic lateral 
sclerosis. 1, anterior horns of gray matter containing the trophic cells; 2, crossed 
pyramidal tracts; 3, the direct pyramidal tract. 

Spinal Pachymeningitis. — Spastic paraplegia may also be due to 
spinal pachymeningitis, and the associated symptoms may so closely 
resemble those of myelitis that a differential diagnosis is impossible; 
but the spastic character of the paraplegia, the early appearance 
and severity of the pain, and the comparatively slow development 
of the symptoms in pachymeningitis will aid in separating the two 
affections, as will also the presence of persistently increased reflexes 
from the first. Sensory disturbances, aside from pain, are common 
in myelitis, but rare in this condition. If the inflammatory process 
becomes widespread there may be sensory disorders and trophic 
sloughs, owing to invasion of the portions of the cord connected 
with sensation and nutrition by a secondary myelitis. The develop- 
ment of signs of spinal caries, sepsis, or a psoas abscess in such 
cases at once shows the condition to be meningeal in origin, and 
the history of traumatism will point to meningitis, rather than 
myelitis. 

Spinal Syphilis. — Spastic paraplegia, greatly increased tendon 
reflexes, low muscle tension, vesical disorder, and slight sensory 



PARAPLEGIA 87 

disturbances in an adult should make the physician think of 
spinal syphilis. 

Pott's Disease. — Spastic paraplegia in early childhood, when not 
due to cerebral lesions, as already discussed, is usually due to Pott's 
disease. The reflexes are exaggerated, the hands are drawn up, 
and the feet are extended. Inquiry will perhaps reveal a history 
that the child has been easily tired before the paralysis came on, 
and has complained of belly-ache, which has really been due to pain 
along the intercostal nerves from the irritation at their roots. The 
area of the cord involved can be determined by the symptoms as 
detailed on pages 91 and 92. The prognosis is not always unfavor- 
able, as extraordinary recoveries take place. 

Hysteria. — An important form of contracture following paralysis 
or occurring without it, prone to lead to a mistake in diagnosis, 
is that seen in hysteria. As a rule, the contractures come on in 
association with paraplegia. Sometimes, however, they affect the 
arms or an arm, one leg or both legs. It is a characteristic of these 
contractures due to hysteria that they set in suddenly, and are 
often accompanied by such hysterical symptoms as borborygmi, 
ovarian tenderness, and often areas of anesthesia. Weir Mitchell 
has divided these cases into two forms. The first only involves 
single parts or limited muscle groups, and, though the contractures 
may last for years, joint or muscle changes do not occur. In the 
second class, one limb after another is attacked until all means of 
locomotion, or even moving the trunk, are lost, and the muscles, 
joints, and areolar tissue undergo organic changes. The reflexes 
are lost in such cases in the late stages, and the electrical reaction 
of the muscles is impaired. The diagnosis is to be reached by the 
sex, the persona] history, the history of the illness, the presence of 
anesthesia (see chapter on Skin), and hyperesthesias. Usually the 
contracture comes on suddenly; it is very rigid, and the muscles 
on both sides of the limb are fixed — that is, the contracture involves 
antagonistic muscles. Sleep does not always cause a relaxation of 
hysterical contraction, but ether or chloroform usually does so. 
(See chapter on the Hands and Arms.) 

Transverse Myelitis. — In transverse myelitis there is often in 
the later stages of the malady spastic parap]egia as a result of the 
irritability of the spinal centres below the seat of the lesion, which 
may cause a spastic state of the muscles. In distinction from 
lateral sclerosis we find in myelitis that there is loss of power in the 
bladder and rectum, sensory paralysis and muscular atrophy. 

Non-spastic Paraplegia. — -Passing from spastic paraplegia we 
come to those forms of paraplegia lacking this peculiarity. They 
are quite numerous and important. If the paraplegia comes on 
suddenly the cause may be hemorrhage into the substance of the 
cord or into the spinal membranes, or be due to compression or 



88 THE FEET AND LEGS 

destruction of the cord by injuries of the back, whereby there 
is laceration of the soft parts or fracture or dislocation of the 
vertebrae, or it may be due to acute transverse myelitis. 

When the paraplegia is slower in onset but not sudden, the spinal 
causes are acute transverse myelitis, acute ascending paralysis or 
Landry's paralysis, and acute central myelitis. On the other hand, 
the slowly oncoming non-spastic paraplegias are due to chronic 
myelitis, to locomotor ataxia, poliomyelitis, neuritis, and pressure 
due to disease of the vertebrae or to spinal tumors. Finally we 
have what are called reflex and hysterical paraplegias. 

Myelitis. — By far the most common cause of paraplegia is mye- 
litis in one of its forms; but whether the onset be rapid or slow, 
it must be remembered that the symptoms of myelitis depend, 
first, upon the level at which the spinal cord is involved, and, 
second, upon whether the lesion involves the white matter or the 
gray. If the lesion is an acute central myelitis of the gray matter, 
it usually produces many of the symptoms about to be detailed 
under acute transverse myelitis, but the onset is malignant and 
the areas involved are usually widespread. It is attended by fever 
of a marked type, though the temperature of the paralyzed parts 
is below normal, and by early evidences of trophic lesions. Multiple 
arthritis may come on. The bladder and rectum are paralyzed, 
and, finally, delirium may develop. The prognosis is unfavorable. 
Acute central myelitis is to be separated from Landry's paralysis 
by the facts that in it sensation is lost, and there are rectal 
and vesical paralysis, and rapid trophic changes. From poly- 
neuritis it is separated by the facts that there are no great trophic 
changes in this form of neuritis, and the rectum and bladder are 
rarely paralyzed. 

The symptoms of acute transverse myelitis are capable of being 
divided into three groups, in the first of which the onset is as sudden 
as is that of apoplexy, in the second the symptoms come on quickly, 
and in the third, more subacutely. In the acute forms, however, 
the history will be that after a period of numbness, heaviness, and 
weakness of the legs, with more or less pain in the back, the patient 
has found it impossible to move his legs, has lost control of his 
bladder and rectum, or suffers from retention of the urine and feces 
instead, and at the same time has developed anesthesia of his lower 
extremities and the girdle sensation, or, if the lesion be situated 
high up in the cord, tingling in his arms. (See chapter on the Skin.) 
The reflexes may be abolished at first, and then return in an exag- 
gerated form in the segments of the cord below the area affected. 
In other cases the reflexes do not return if the lesion is completely 
transverse. The patient is speedily bedridden, and to these symp- 
toms just detailed is soon added the development of bed-sores and 
sloughs on dependent parts of the legs or on the buttocks, followed, 



PARAPLEGIA 30. 

it may be, by death from exhaustion, although the case may survive 
for months and even become somewhat better. If improvement 
takes place, sensation returns in the course of from one to six 
months, some motion in from six to eighteen months, and, finally, 
spasms and contractures may result from descending degeneration 
of the lateral tracts. 

In cases in which paraplegia results from the more subacute form 
of transverse myelitis the symptoms are not quite so rapid in their 
onset as in the type just named. The patient first notices that 
his bladder and rectum are unduly irritable, and in his limbs there 
may be subjective sensory disturbances. (See Paresthesia, in 
chapter on the Skin.) The motor symptoms begin by a feeling of 
heaviness or inability to quickly move the lower limbs, so that the 
patient feels tired on slight exertion. Soon these symptoms deepen 
into absolute anesthesia and motor paralysis, and the girdle 
sensation on the trunk becomes well developed. (See chapter on 
the Skin.) The bladder, which at first was irritable, may now be 
toneless, paralyzed, and retentive or incontinent: retentive if the 
lesion is above the lumbar cord, and incontinent when the lower 
part of the lumbar enlargement is diseased. The reflexes at first 
may be abolished, but very soon some of them return, only those 
reflexes the centres for which are destroyed by the transverse 
lesion being abolished; that is, the reflexes recover after the first 
shock of the attack, and those muscles and tendons having spinal 
centres below the lesion have their reflexes increased because they 
are cut off from the inhibiting centres higher up in the cord or 
medulla. The muscles of the legs, which at the first shock of the 
onset of the malady were all flaccid and paralyzed, now divide 
themselves into two classes: those that are connected with the 
diseased part of the cord, which remain paralyzed, and those which 
are connected with the lower centres, which recover some power; 
but as the lesion is so placed as to cut off all of them from cerebral 
influences, voluntary motion is lost as completely as if all were 
deprived of spinal influence. The truly paralyzed muscles waste, 
but the others which have unimpaired spinal centres do not, except 
very slowly from disuse. On the contrary, they often become 
spastically contracted. Other trophic changes, such as bed-sores 
and bullae, develop in the skin connected with the diseased focus, 
but not in the skin connected with centres below the lesion. Anes- 
thesia is present because the lesion prevents the sensory impulse 
from reaching the brain. (See chapter on the Skin.) 

The following diagram from Seymour Taylor's Index of Medicine 
presents the symptoms of a lesion in the spinal cord in transverse 
myelitis: 



go 



THE FEET AND LEGS 



Symptoms in Transverse Myelitis. 

The darkened portion represents the seat of lesion. 

Spinal cord. 



Reflexes normal 



Band of hyperesthesia .... 

Muscles palsied, waste, and lose 
their electrical reactions . . 

Reflexes lost ........ 

Sensation lost ....... 

Muscles palsied ...... 

Do not waste 

No loss of electrical reactions . 

Reflexes increased 

Sensation lost ....... 

Bedsores 

Temperature above rest of body 




Reflexes normal. 

Band of hyperaesthesia. 

Muscles palsied, waste and lose 
their electrical reactions. 

Reflexes lost. 

Sensation lost. 

Muscles palsied. 

Do not waste. 

No loss of electrical' reactions. 

Reflexes increased. 

Sensation lost. 

Bedsores. 

Temperature above rest of body. 



When the entire cord is not evenly involved in the transverse 
lesion certain groups of muscles partly escape. It is asserted that 
the extensors escape oftener than the flexors. The height of the 
paralysis also depends upon the situation of the lesion of the cord, 
and if high enough to involve the cervical region, and yet not high 
enough to paralyze the diaphragm and cause death (third or fourth 
cervical), there may be contraction of the pupil by involvement 
of the fibres from the nucleus of the third nerve, which runs down 
the cord to the last cervical vertebrae before joining the sympathetic. 

The symptoms of chronic transverse myelitis producing paraplegia 
are practically identical with the more acute form just described, 
except that they are very slow in their development. 

The Seat of the Lesion. — Having discussed the various forms of 
myelitis, we have still to study the question of the seat of the lesion. 
Before doing this, it is to be remembered, in studying the relation- 
ship of the spinal cord to the vertebras, that the so-called segments 
of the cord in no way correspond with the various segments of the 
spinal column bearing similar names. Thus the cord extends only 
to the level of the upper part of the second lumbar vertebra, 
although the spinal canal reaches much lower than this. There 
are thirty-one segments of the cord, each of which gives off a 
pair of spinal nerves. The first segment of the cord is at the 



PARAPLEGIA 



91 



foramen magnum and the last 
at the second lumbar vertebra. 

This is well shown in the ac- 
companying figure, modified from 
one by Gowers (Fig. 25). 

Not only is this true, but the 
nerves do not emerge from the 
spinal canal where they leave the 
cord, but at a lower level. In the 
case of the lumbar and sacral 
segments of the cord the nerves 
form a bundle which extends 
down the remaining part \)f the 
spinal canal. 

There are two areas in the cord 
of greater importance than the 
others, namely, the cervical en- 
largement, which gives off the 
nerves to the upper extremities, 
and the lumbar enlargement, 
which supplies the lower extremi- 
ties. The eighth cervical and 
first dorsal segments of the cord 
lie opposite the spine of the 
seventh cervical. vertebra and the 
lumbar-sacral enlargement oppo- 
site that of the spine of the tenth 
dorsal vertebra. 

Let us suppose that a patient 
presents himself with the follow- 
ing condition : There is complete 
paralysis of his arms and legs, 
with paralysis of the muscles of 
the trunk, and total anesthesia 
of the same areas. The legs are 
in a state of spastic paralysis, 
their reflexes are increased, and 
their nutrition is unimpaired; 
although the arms are found re- 
laxed and flaccid, devoid of reflex 
excitability, and undergoing de- 
generative atrophy. The bladder 
and rectum are not retentive. 
All these symptoms point to a 
transverse lesion of the spinal 
cord in the cervical region, prob- 
ably between the fifth cervical 




Fig. 25. — Showing relation of seg- 
ments of cord to vertebrae and rela- 
tion of spinal nerve roots to the cord 
and their levels of exit (modified from 
Gowers). The figures to the left refer 
to the spines of the vertebrae, the next 
column of figures to the segments of 
the cord, the next column to the bodies 
of the vertebrae, and the last figures to 
the right to the spinal nerves. 



Q2 



THE FEET AND LEGS 



and first dorsal vertebrae. If, on the other hand, the upper 
extremities are not affected (except, perhaps, the small muscles 
of the hand), but there is the same loss of power in the legs, 
with spastic contraction of the muscles, and the other symptoms 
just named are present, combined with degeneration of the muscles 
of the trunk, the lesion is probably somewhere between the second 
and twelfth dorsal vertebrae. 

Again, if the paralysis of motion and sensation be only in the 
lower limbs, and there be flaccidity of the muscles (where before 
we discovered spastic contraction), with muscular degeneration, 
loss of reflexes, and paralysis of the bladder and rectum, the lesion 
is between the tenth dorsal and first sacral vertebra. 

Still further, if there be loss of power with degeneration of the 
small muscles of the feet, and loss of sensation of the outside of 
the feet and toes, and of the skin about the anus, with preservation 
of power in the thighs and of the patellar reflex, the lesion is at the 
end of the cord in the area of the cone. 

In this connection the reader should study that part of the 
chapter on the Skin which deals with anesthesia. 

Differential Diagnosis of Lumbar, Dorsal, and Cervical 
Myelitis. 1 



Paralysis. 



Sensation. 



Atrophy. 



Electrical 
reaction. 



Bladder. 



Bowels. 



Reflexes, 
superficial. 

Reflexes, 
deep. 

Priapism. 



Lumbar myelitis. 



Paraplegia. 



Pains in legs, or girdle-pains 
around loins; hyperesthetic 
zone around loins; anes- 
thesia of legs, complete 
or uneven distribution. 



Of legs. 



R. D. in atrophied muscles; 
or in mild cases quantita- 
tive diminution. 



Incontinence from paralysis 
of sphincter. 



Incontinence from paralysis 
of sphincter; disguised by 
constipation. 

Lost. 



Lost. 

Absent. 



Dorsal myelitis. 



1. Dorsal, abdominal, and 
intercostal muscles, ac- 
cording to height of lesion. 

2. Legs. 

Girdle-pain and hyperes- 
thetic zone between ensi- 
form cartilage and pubes. 



Of dorsal and abdominal 
(and intercostal muscles 
not subject to examination) 
corresponding to height of 
lesions; sometimes mild 
and slow of legs. 

R. D. in dorsal and abdomi- 
nal muscles; slight quanti- 
tative changes only in legs 
when wasted. 

Retention, or intermittent 
incontinence from reflex 
action; later from over- 
flow. Cystitis common. 

Involuntary evacuation 
from reflex spasm or con- 
stipation. 

Temporary loss, then rapid 
increase. 

Temporary loss, then slow 
increase. 



Often present. 



Cervical myelitis. 



Neck-muscles, dia- 
phragm, arms, trunk, 
and legs. 



Hyperesthesia and 

pains in certain 
nerve -distributions 
of arms; below this 
anesthesia of arms, 
body, and legs. 

Atrophy of neck-mus- 
cles (rare) or more 
commonly of arms. 



R. D. in atrophied 
muscles. . 



Same as in dorsal mye- 
litis. 



Same as in dorsal mye- 
litis. 



Same as in dorsal mye- 
litis. 

Same as in dorsal mye- 
litis. 



Often present. 



1 From Prince's article in Dercum's Nervous Diseases. 



PARAPLEGIA 



93 



Localization of the Functions of thr Segments of the Spinal 
Cord. (According to Starr ) 



Segment. 



Muscles. 



II. and III 

Cervical. 



IV. 

Cervical. 



Cervical. 



VI. 
Cervical. 



VII. 

Cervical. 



VIII. 

Cervical. 



I. Dorsal. 



II. to XII. 

Dorsal. 



I. Lumbar. 



II. 
Lumbar. 



Sterno-mastoid. 
Trapezius. 
Scaleni and neck. 
Diaphragm. 

Diaphragm. 

Deltoid. 

Biceps. 

Coraco-brachialis. 

Supinator longus. 

Rhomboid. 

Supra- and infra spinatus. 

Deltoid. 

Biceps. 

Coraco-brachialis. 

Brachialis anticus. 

Supinator longus. 

Supinator brevis. 

Rhomboid. 

Teres minor. 

Pectoralis (clavicular part). 

Serratus magnus. 

Biceps. 

Brachialis anticus. 

Pectoralis (clavicular part). 

Serratus magnus. 

Triceps. 

Extensors of wrist and 

fingers. 
Pronators. 

Triceps (long head). 
Extensors of wrist and 

fingers. 
Pronators of wrist. 
Flexors of wrist. 
Subscapular. 
Pectoralis (costal part). 
Latissimus dorsi. 
Teres major. 

Flexors of wrist and fingers 
Intrinsic muscles of hand. 

Extensors of thumb. 
Intrinsic hand muscles. 
Thenar and hypothenar 
eminences. 

Muscles of back and abdo- 
men. 
Erectores spinee. 



Ilio-psoas. 
Sartorius. . 
Muscles of abdomen. 



Ilio-psoas (sartorius). 
Flexors of knee (Reraak). 
Quadriceps femoris. 



Hypochondrium. (?) 

Sudden inspiration produced 
by sudden pressure beneath 
the lower border of ribs. 

Pupil. 4th to 7th cervical. 

Dilatation of the pupil pro- 
duced by irritation of the 
neck. 



Scapular. 

5th cervical to 1st dorsal. 

Irritation of skin over the 
scapula produces contrac- 
tion of the scapular mus- 
cles. 

Supinator longus. 

Tapping its tendon in wrist 
produces flexion of fore- 



Triceps. 

5th to 6th cervical. 

Tapping elbow tendon pro- 
duces extension of forearm 

Posterior wrist. 

6th to 8th cervical. 

Tapping tendons causes ex- 
tension of hand. 

Anterior wrist. 
7th to 8th cervical. 
Tapping anterior tendons 

causes flexion of wrist. 
Palmar. 7th cervical to 1st 

dorsal. 
Stroking palm causes closure 

of fingers. 



Epigastric. 4th to 7th dorsal. 

Tickling mammary region 
causes retraction of the 
epigastrium. 

Abdominal. 7th to 11th dor- 
sal. 

Stroking side of abdomen 
causes retraction of belly. 

Cremasteric. 2d to 3d lum- 
bar. 

Stroking inner thigh causes 
retraction of scrotum. 

Patellar tendon. 
Striking tendon causes ex- 
tension of leg. 



Sensation. 



Back of head to vertex. 
Neck. 



Neck. 

Upper shoulder, 

Outer arm. 



Back of shoulder and 

arm. 
Outer side of arm and 

forearm, front and 

back. 



Outer side of forearm, 

front and back. 
Outer half of hand. 



Inner side and back of 
arm and forearm. 

Radial half of the 
hand. 



Forearm and hand, 
inner half. 

Forearm, inner half. 
Ulnar distribution to 
hand. 



Skin of chest and 
abdomen, in bands 
running around and 
downward corre- 
sponding to spinal 
nerves. 

Upper gluteal region. 



Skin over groin and 
front of scrotum. 



Outer side of thigh. 



94 



THE FEET AND LEGS 



Localization of the Functions of the Segments of the Spinal 
Cord. (According to Starr.) (Continued.) 



Segment. 


Muscles. 


Reflex. 


Sensation. 


III. 
Lumbar. 


Quadriceps femoris. 
Inner rotators of thigh. 
Abductors of thigh. 


Front and inner side 
of thigh. 


IV. 

Lumbar. 


Abductors of thigh. 
Adductors of thigh. 
Flexors of knee (Ferrier). 
Tibialis anticus. 


Gluteal. 

4th to 5th lumbar. 
Stroking buttock causes 
dimpling in fold of buttock. 


Inner side of thigh and 

leg to ankle. 
Inner side of foot. 


V. 

Lumbar. 


Outward rotators of thigh. 
Flexors of knee (Ferrier). 
Flexors of ankle. 
Extensors of toes. 




Back of thigh, back of 
leg, and outer part of 
foot. 


I. to II. 

Sacral. 


Flexors of ankle. 

Long flexor of toes. 

Peronei. 

Intrinsic muscles of foot. 


Plantar. 

Tickling sole of foot causes 
flexion of toes and retrac- 
tion of leg. 


Back of thigh. 
Leg and foot, outer 
side. 


III. to V. 
Sacral. 


Perineal muscles. 


Foot reflex, Achilles tendon. 
Overextension of foot causes 
rapid flexion; ankle clonus. 
Bladder and rectal centres. 


Skin over sacrum. 

Anus. 

Perineum. Genitals 



8th cervical and 1st dor 
sal segment at 7th ver 
tebra. 



Lumbar enlargement o 
cord at 10th dorsal ver 
tebra. 



End of cord at 2d lumbar 
vertebra. 



Cauda equina.— — 




1st to 7th cervical 
vertebra. 



1st to 12th dorsal 
vertebra. 



1st to 5th lumbar 
vertebra. 



1st to 5th sacral 
vertebra. 



Fig. 26. — Showing the surface areas of the back corresponding approximately 
to the areas of the spinal cord supplying the trunk and limbs, according to the 
diagram on the preceding page. 



PARAPLEGIA 95 

This subject is still further subdivided and elucidated by the 
preceding table and by Fig. 26. 

Finally, it is possible for disease of the cauda equina to produce 
symptoms of a lumbar-sacral lesion, owing to the fact that this 
bundle is composed of fibres derived from these two areas. The 
patellar reflex may be preserved, as the lesion is below the reflex 
arc, and all the fibres may not be involved. 

Locomotor Ataxia. — Paraplegia when due to locomotor ataxia is 
nearly always so surrounded by other typical symptoms of this 
disease as to render easy its separation from the paraplegia of 
myelitis, and, further, there is rarely a true loss of power. The 
stabbing and darting pains of ataxia (see chapter on Pain), the 
presence of the Argyll-Robertson pupil, the absence of the patellar 
reflex, and the atrophy of the optic nerve are all characteristic of 
ataxia, and are absent in myelitis. (See early part of this chapter 
on Gait.) 

Ataxic Paraplegia. — The symptoms of lateral sclerosis and amyo- 
trophic lateral sclerosis have already been discussed under Gait 
and Spastic Paraplegia, but in the paraplegia called ataxic para- 
plegia, also already discussed, there are in association lateral sclero- 
sis and posterior sclerosis, and for this reason some of the symptoms 
of both are found to be present. Thus, in addition to loss of power 
there is a spastic condition of the legs with exaggerated reflexes, 
absence of the Argyll-Robertson pupil and of crises of pain, but 
the Romberg symptom, or swaying when the eyes are closed, is 
present. The condition which most closely resembles ataxic para- 
plegia is that of tumor of the middle lobe of the cerebellum, but in 
such cases we have, in addition, headache, vertigo, optic neuritis, 
titubation, and sometimes vomiting. 

Poliomyelitis. — The onset of paraplegia in a young child, pre- 
ceded by an attack of fever, vomiting, restlessness, and general 
illness, lasting but a few hours or days, and which may be compli- 
cated by convulsions, all point to the cause being poliomyelitis of a 
severe type. The legs are, however, as a rule, only completely 
paralyzed for a brief period after the attack. Eventually the storm 
clears off, and only the muscles directly connected with the diseased 
cells in the cord (anterior cornua) remain paralyzed. There is no 
loss of sensation, but reflex action is abolished in the paralyzed 
parts. Far and away the most important point in the diagnosis is 
the symptom of rapid wasting of the muscles in the paralyzed parts 
and the rapid development of coldness in these areas, which is due 
to the destruction of the trophic centres in the spinal cord. (See 
Fig. 27.) (See Monoplegia.) 

Paraplegia Resulting from Tumor of the Cord or its membranes 
only ensues when the growth is so placed as to cut off all the motor 
tracts supplying both limbs, which is rarely accomplished until 



96 THE FEET AND LEGS 

after a long history of more or less wel] -developed motor and sensory 
failure. The paralysis is developed in the areas supplied by the 
centres in the cord below or at the level of the growth, and the 
violent pain nearly always present in cases of tumor points to 
the diagnosis. Very painful paraplegia, therefore, indicates spinal 
tumor as its cause. The areas of anesthesia and the muscles 
involved may also give definite information as to the seat of the 
growth. (See chapter on the Skin, and Starr's table just quoted.) 

Hemorrhage into the Spinal Cord. — Hemorrhage into the spinal cord 
is an exceedingly rare condition unless preceded by grave disease 
of its tissues. Indeed, the existence of such a condition in man has 
been denied. The patient, previously in good health, is stricken 
suddenly to the ground, and there may be almost as much cerebral 
disturbance as in cerebral apoplexy, but consciousness is generally 
preserved. The amount of paraplegia may be instantly complete, 
or not be complete for twenty-four hours. Bed-sores speedily 
develop, and death ensues from exhaustion or from extension of 
the hemorrhage upward to the vital centres. Practically identical 
symptoms ensue when the hemorrhage takes place between the 
membranes covering the cord. In both instances the reflexes are 
lost if the hemorrhage be sufficient to produce total paralysis. 

Acute Ascending Myelitis. — If, on the other hand, after a pro- 
dromal period of short duration, during which there is some fever, 
the patient is suddenly attacked with paraplegia, the cause may 
be the acute ascending myelitis of Landry, and the rapid extension 
to the trunk, the arms, and the respiratory muscles, with the con- 
sequent early death of the patient, will confirm the diagnosis. 
There is usually no involvement of sensation or trophic changes, 
and the sphincters of the bladder and rectum escape the paralysis. 
Landry's paralysis is very rare. Similar symptoms associated with 
sensory disturbances are probably due to a polyneuritis. 

Diller and Meyer state that the cardinal points for diagnosis of 
Landry's paralysis are: 

i. Flaccid paralysis of the muscles, spreading rapidly from one 
point over the rest of the body, generally beginning in' the legs, but 
sometimes following the reverse order, as in the French zoologist, 
Cuvier. 

2. Absence of muscular atrophy and of electrical reaction of 
degeneration (patient dies before there is time for them to develop) . 

3. Tendon and superficial reflexes absent. 

4. Sensibility not, or only slightly, impaired. 

5. Sphincters, as a rule, intact (exceptions rather frequent). 
Fracture of Vertebrae. — If the paraplegia be due to compression 

from fracture or dislocation of the vertebrae or to other direct 
injury the history of the patient, the evidences of external local 
mischief, and an x-ray examination will decide the diagnosis. 



PARAPLEGIA 97 

Reflex Paralysis. — Very rarely during the course of severe disease, 
producing irritation of the bladder, kidney, bowels, or rectum, as 
in violent cystitis, stone in the kidney, and dysentery, paraplegia 
comes on, due in some cases to an infectious myelitis, but in others 
to what is apparently only a reflex paralysis, as it often passes away 
with the removal of the source of irritation. Even worms in the 
intestine are said to have produced such a paralysis, and their 
removal has been followed by cure. Generally sensation in the 
limbs is unimpaired and the bladder and rectum act normally. 
Sometimes, however, in the presence of severe renal disease, as 
renal calculus, there may be all sorts of disturbances of sensation 
and pain, as well as great motor paralysis, with total loss of reflexes, 
following an exaggeration of the reflexes. Probably these severe 
cases are always due to a coincident myelitis rather than to a 
reflex irritative cause. 

Hysteria. — No form of paraplegia presents so many types or 
simulates so many organic diseases as does that due to hysteria, 
for there may be not only great loss of motion, but exaggerated 
reflexes, relaxation or spastic contraction of the muscles, anesthesia 
and hyperesthesia, pain or no pain. The very occurrence of such 
irregular manifestations in a young, neurotic girl, the fact that the 
anesthetic areas in some cases, constantly tend to shift their 
position, and, finally, that the contractures, if present from hysteria, 
disappear on administering an anesthetic to a stage in which mus- 
cular relaxation is produced in the ordinary individual, aid us in 
making a diagnosis. 

(See that part of this chapter on Contractures and the text on 
Anesthesia of the Skin.) 

Scurvy. — A pseudoparalysis of the legs with immobility some- 
times occurs as a symptom of scorbutus in infancy. The parents 
notice that the child flinches when it is picked up or handled, and 
seems as if tender from rheumatism. Often the gums are swollen 
and bleeding, and purpuric eruptions appear on the skin. The 
shafts of the bones of the legs or of the arms may be enlarged, 
and hematuria or bloody stools may appear. 

Rickets. — Pseudoparaplegia may also occur in rickety children 
from faulty muscular and bony development. It is to be separated 
from the ordinary paraplegias of childhood by the state of the bones, 
the presence of knee-jerks, and the absence of local wasting or spasm, 
although general spasms, or carpopedal spasm, are often seen in 
rickety children. 

Diphtheritic Paralysis. — Not uncommonly a partial paraplegia 
occurs as a result or sequel of diphtheria. The condition, however, 
is more ataxic than paraplegic, and Bourges asserts that there is no 
muscular atrophy such as occurs in true paraplegia due to neuritis, 
or in that due to some spinal lesions. 
7 



9» THE FEET AND LEGS 

Neuritis. — When neuritis produces sudden paraplegia the symp- 
toms very closely resemble those of acute myelitis. Neuritis may 
also cause pseudotabes if its onset is slow. The neuritis is always 
multiple and involves the arms and the body after affecting the legs; 
there is usually well-developed anesthesia (see chapter on the Skin) , 
preceded by sensory disturbances and marked muscular and nerve- 
trunk tenderness; but there is no girdle sensation, as there is in 
myelitis and tabes. There are often trophic changes in the skin 
in neuritis (see chapter on the Skin), but no bed-sores as in myelitis. 
J. M. Da Costa stated that malarial neuritis may cause paraplegia 
of the lower limbs, but, as a rule, toxic neuritis produces also loss of 
power in the arms. Very rarely paraplegia of the lower extremities 
results from diabetes mellitus, the lesion being in all probability 
multiple neuritis. 

Family Periodic Paralysis. — A very rare condition, involving not 
only the legs, but the entire body, is what is called family periodic 
paralysis, in which flaccid motor paralysis, with loss of electrical 
reaction and reflex activity, comes on suddenly, lasts for a few 
hours or days, and is then followed by perfect health. It is 
always hereditary. 

MONOPLEGIA. 

Monoplegia of a Lower Extremity may be due to a cerebral lesion 
or of spinal or nerve-trunk lesions. The cerebral lesion producing 
monoplegia in one leg is very rare, and if it occurs, at any age, indi- 
cates a lesion in the convolutions at the upper end of the fissure of 
Rolando, and the continuation of this area in the paracentral lobule 
of the marginal convolution. If there are no signs of cerebral 
trouble, the presence of a complete leg monoplegia can mean one of 
several things, namely, a lesion limited to one side of the cord, as, 
for example, a hemilateral myelitis, hysterical paralysis, in which 
there will be irregular anesthesia (see chapter on the Skin) , and the 
other hysterical signs, or a tumor pressing on the crural nerve in the 
pelvis, or section of the nerve by injury. Apparent monoplegia 
may, however, be due to muscular pain or a painful phlebitis 
producing muscular fixation. 

If the condition is due to a lesion on one side of the cord, the 
symptoms are quite characteristic. There is paralysis of all the 
muscles of the leg which are supplied by the part of the cord affected 
or below it. The muscles, the nerve supply of which comes directly 
from the affected part, eventually waste and undergo degenerative 
changes. The most typical symptom of this lesion is, however, the 
crossed character of the sensory paralysis. That is to say, there is 
loss of sensation in the limb opposite that in which motion is lost, 
and in the limb, in which motion is lost there is hyperesthesia, so 



MONOPLEGIA 



99 



that the lightest touch may be very painful. The cause of this is 
obscure, for the studies of Mott have proved that the sensory tracts 
in the cord do not decussate on entering it, as has been supposed 
heretofore. There is, however, a symmetrical band of anesthesia 
around the body at the level of the lesions, and a similar band of 
hyperesthesia above the lesions. The reflexes of the parts supplied 
by the diseased area are lost, but those supplied by the area below 
the lesions are increased as in ordinary myelitis. Very commonly 
the paralyzed limb is overwarm from vasomotor palsy. 

Diagram showing Symptoms in Hemilateral Myelitis. 1 

(The darkened mass represents the site of the lesion.) 

Spinal cord. 



Reflexes normal 

Band of hyperesthesia .... 

Band of anaesthesia 

Reflexes lost 

Motor palsy 

Hyperesthesia 

Reflexes increased ..... 

Temperature above that of the 
rest of the body 



I 



Reflexes normal. 
Band of hyperesthesia. 
Band of anaesthesia. 

Motor power unaffected. 

Anesthesia. 

Reflexes unaffected. 

Temperature same as that of 
the rest of the body. 



Paralysis of Certain Groups of Muscles or a single muscle in the 
legs is most commonly due to anterior poliomyelitis or neuritis 
(Fig. 27). In poliomyelitis the child will be found to have loss of 
power in certain muscles in one or both legs (see also Paraplegia), 
so that there is a dragging of the toe, or " foot-drop," the shoe 
becomes irregularly worn through, being dragged on one edge along 
the ground, the involved muscles being peculiarly relaxed and 
flaccid, so that the leg may wabble, to use a crude term. This is 
sometimes called a " Punchinello leg." There is no tendency to 
spastic contraction, the reflexes are rapidly lost in the affected part, 
and the muscles speedily waste and develop the reaction of de- 
generation. When contractures take place they are not spastic, 
but are due to healthy muscles being unopposed by the diseased 
ones. The temperature of the paralyzed part is lower than normal. 
Sometimes muscular atrophy may be masked in young children by 
the abundance of subcutaneous fat. A point of some importance 
in examining the reflexes is that presence of knee-jerk should not 
exclude the diagnosis of poliomyelitis, because the reflex act is 

1 From Seymour Taylor's Index of Medicine. 



IOO THE FEET AND LEGS 

only destroyed if the centres which are concerned in this jerk are 
diseased — that is, if the disease has affected only that part of the 
cord supplying the foot, a tap on the knee may readily produce a 
response, whereas if the disease be higher up on the cord the reflex 
will be lost. The chronic anterior poliomyelitis of adult life pre- 
sents very similar symptoms to the acute form of infancy, but is a 
very rare disease. 




Fig. 27. — Areas involved in acute and chronic poliomyelitis. In children it is 
sometimes called acute infantile paralysis. The shaded area indicates the cells 
in anterior cornua of gray matter which are involved. 

Care must be taken that paralysis of the leg resulting from an 
injury to the peroneal nerve with resulting neuritis is not mistaken 
for acute poliomyelitis. The history of an accident, or pain, swell- 
ing, and the presence of a bruise aid us in making a diagnosis. 
If these symptoms occur in an adult, a possible cause is paralysis 
of the peroneal nerve occurring in the course of tabes. (In connec- 
tion with this chapter see that on the Significance of Anesthesia of 
the Skin.) 

Spastic Monoplegia or Single Contracture. — Spastic mono- 
plegia may arise from several causes. (1) A shrivelled, undeveloped 
foot and leg with drawing up and deformity are seen most com- 
monly as the ultimate result of the acute cerebral paralysis of 
infancy. (2) Deformity or distortion of the legs may result from 
the secondary muscular atrophy following upon chronic inflam- 
mation in a joint or joints. The muscular wasting under these 
circumstances may arise from neuritis, which is associated with 
the arthritis, but its cause is often difficult to discover. It may 
develop as a manifestation of progressive muscular atrophy in 



DEFORMITIES OE THE FEET AND LEGS IOI 

those rare cases in which the disease begins first in a lower limb, 
the so-called peroneal, or leg, form of the disease. The extensor 
muscles of the toes lose their power, the interossei waste, the foot 
may be flattened or claw-shaped, or, in other instances, any one of 
the forms of club-foot may develop. If the deformity is bilateral, 
it is a strong evidence of its being the leg type of progresssive 
muscular atrophy, and that it is not due to acute infantile paralysis. 
There will probably be a history of heredity in such cases. This 
state of the foot must be carefully separated from the pes equinus 
seen as a result of acute infantile spinal paralysis involving the 
tibialis anticus. The toes are hyperextended, and the foot is very 
broad when viewed from side to side at the metatarsal joints. It 
is stated that this sign is considered characteristic of the early 
development of the disease in families with the heredity. Some- 
times in place of this deformity the foot becomes almost parallel 
with the tibia in excessive extension, with eversion as the result of 
shortening of the peroneus longus. In other instances the deform- 
ities undergo marked changes as the disease progresses, so that 
they not only grow worse, but are altered in type. In distinction 
from ordinary progressive muscular atrophy this leg type often 
has marked disturbance of sensation associated with it. (Dana.) 
It generally occurs in males. According to Marie, another form of 
claw-foot is seen in Friedreich's ataxia, there being associated with 
it club-foot. 

Progressive muscular atrophy of the peroneal type is a rare 
disease, which must be separated from multiple neuritis by the 
pain of the latter affection and the fact that neuritis rarely pro- 
duces double club-foot, and, further, that in neuritis there is no 
history of heredity. From poliomyelitis we separate it by the fact 
that in this peroneal type of paralysis the onset is more slow and 
by the fact that there is a loss of the reflexes in severe poliomyelitis, 
though they are preserved for a long time in the peroneal type. 
From Friedreich's ataxia it is separated by the fact that in that 
rare disease the reflexes are lost, there is a peculiar unsteadiness 
in walking, and an absence of electrical changes in the muscles. 



DEFORMITIES OF THE FEET AND LEGS. 

Much of what has been said in the preceding chapter as to the 
disease which produce alterations in the shape of the hand and arm 
applies equally to the changes from the normal seen in the appear- 
ance and movements of the feet and legs. The feet are greatly 
enlarged symmetrically in acromegaly and in Marie's pulmonary 
osteo-arthropathy. In the latter disease the enlargement is par- 
ticularly noticeable because it is the extremities which are chiefly 



102 THE FEET AND LEGS 

hypertrophied, whereas in acromegaly there is simultaneous 
enlargement of the shafts of the long bones. (See chapter on the 
Hands and Arms.) It is to be remembered that in both acromegaly 
and pulmonary osteo-arthropathy the enlargement seems to be 
due to hypertrophy of all the tissues composing the foot, whereas, 
on the other hand, in myxedema the foot, though enlarged, is 
puffed and swollen in appearance through increase of the sub- 
cutaneous tissues alone. Often the foot appears to be a good deal 
enlarged as the result of deformity, particularly that which consists 
in partial displacement of the articular surfaces of the metatarsal 
and phalangeal bones through the wearing of badly fitting shoes, 
or joint troubles, of which I shall speak later. 

Under the name of " sciopedy" Power has reported a case of 
congenital symmetrical enlargement of the anterior part of the foot 
not involving the heel. Any enlargement of the legs associated 
with this condition, he states, is due to hypertrophy of the muscles 
resulting from the effort to lift the feet. 

In some cases of locomotor ataxia, flat-foot from loss of the plantar 
arch is seen, and various dystrophies of the joints take place as the 
disease progresses. 

Wasting of the muscles of the inner surface of the foot affecting 
the big toe, and those on the outer side involving the movements 
of the little toe, the interossei and the flexor brevis communis, may 
occur from the neuritis due to locomotor ataxia, and as the plantar 
aponeurosis retracts the toes are rendered immovably flexed; in 
other cases in place of flexion there is strong extension. 



THE JOINTS. 

The joints of the lower limbs may be swollen from an arthritis 
arising from many causes, such as septicemia, gonorrheal infection, 
syphilis, acute articular rheumatism, typhoid fever, tuberculosis, 
cerebrospinal meningitis, locomotor ataxia, hemiplegia, rheumatoid 
arthritis (arthritis deformans), acute myelitis, Morvan's disease. 

Gonorrheal Rheumatism. — When arthritis is due to gonorrheal 
infection it is generally seen in the knees or ankles, and occurs in 
men as a rule. It is an infectious arthritis and lasts very persist- 
ently, often attacking at the same time joints so rarely involved 
by rheumatism as the jaw, the vertebral joints, and the sterno- 
clavicular articulation. According to the late Dr. Howard, of 
Montreal, it occurs in five forms: 

(a) Arthralgic, in which there are wandering pains about the 
joints, without redness or swelling. These persist for a long time. 

(b) Rheumatic, in which several joints becomd affected, just as 
in subacute articular rheumatism. The fever is slight; the local 



THE JOINTS 103 

inflammation may fix itself in one joint, but more commonly 
several become swollen and tender. In this form cerebral and 
cardiac complications may occur. 

(c) Acute gonorrheal arthritis, in which a single articulation 
becomes suddenly involved. The pain is severe, the swelling 
extensive and due chiefly to peri-articular edema. The general 
fever is not at all proportinate to the intensity of the local signs. 
The affection usually resolves, though suppuration occasionally 
supervenes. 

(d) Chronic hydrarthrosis. This is usually monarticular, and is 
particularly apt to involve the knee. It comes on often without 
pain, redness, or swelling. Formation of pus is rare. It occurred 
only twice in 96 cases tabulated by Nolen. 

(e) Bursal and synovial form. This attacks chiefly the tendons 
and their sheaths, and the bursae and the periosteum. The 
articulations may not be affected. The bursae of the patella, 
the olecranon, and the tendo Achillis are most apt to be involved. 

Acute Articular Rheumatism. — -Acute articular rheumatism in 
the knee or ankle produces swelling of the joint, redness, heat, 
exquisite tenderness, immobility from pain, swelling of the sur- 
rounding tissues. It does not remain for a long period unchanged 
in one joint, is a process accompanied by fever, and usually modi- 
fied by full doses of the salicylates. 

Acute Synovitis. — Acute synovitis is generally the result of an 
injury, is confined to one joint, is often accompanied by far greater 
effusion into the joint than is seen in rheumatism, and there is no 
systemic disturbance. Should a single joint be affected by an 
aberrant attack of acute rheumatism or synovitis not following 
injury, the physician should never forget the possiblity of its 
being a syphilitic arthritis. 

Locomotor Ataxia. — The most marked alterations in the joints 
are those produced by advanced locomotor ataxia, and are called 
arthropathies. Often they are associated with spontaneous 
fractures of the bones. The knees are most commonly involved, 
then the ankles and hips. A joint or several joints may become 
suddenly swollen usually without pain, and without apparent 
cause, until the swelling becomes quite massive. There are then 
developed osseous hyperplasia and a tendency to dislocation with 
crepitation on movement, and the ends of the bone become worn 
away and absorbed. 

Rheumatoid Arthritis. — In rheumatoid arthritis there is a 
gradual enlargement of the joints from accumulation of fluid, 
which in turn is absorbed, leaving the articulating surfaces rough- 
ened, uneven, and deformed, but there are no deposits of urate of 
sodium as in gout, the deformities being due to alterations in the 
articulating surfaces themselves, and the peri-articular develop- 



104 THE EEET AND LEGS 

ment of bone. The disease always remains in the joint originally 
attacked, although new joints are involved. Pain is often severe, 
complete dislocations and fractures are rare, and the small joints 
are often involved. (See chapter on the Hands and Arms.) 

Rheumatoid arthritis when it progresses to an advanced stage 
causes great deformity by the locking of the joints through the 
development or osteophytes. By the destruction of the cartil- 
ages, wasting of the muscles, and thickening or contraction 
of the ligaments, it may cause false positions of all sorts. In 
the great majority of cases it occurs in women between twenty 
and thirty years of age, but it may develop in early childhood. 
Pain is severe in some cases, absent in others. The thighs become 
flexed upon the abdomen, and the legs on the thighs. The number 
of joints involved varies greatly, but the involvement is generally 
symmetrical. 

Sometimes this disease, which is generally gradual in its onset, 
becomes very acute, speedily involving many joints, causing swell- 
ing of the synovial sheaths and bursae, and being accompanied by 
some febrile movement. The suddenness of its onset, the febrile 
movement when the onset is sudden, and the pain may cause it to 
resemble acute articular rheumatism, but the absence of redness 
in the joints and of the migration of the swelling from one joint to 
another which is the characteristic of acute articular rheumatism, 
aids in the differentiation. 

The Arthritis of Acute Central Myelitis is sudden in its onset, 
generally multiple, and accompanied by the other symptoms of 
that disease. {See Paraplegia and Anesthesia of the Skin.) 

Arthritis of Cerebrospinal Meningitis is a typical infectious 
arthritis, and the presence of the characteristic signs of the disease 
renders its cause evident. The joints are many of them affected 
simultaneously with swelling, pain, and serous or purulent effusions. 

Septic Arthritis. — In cases of septic arthritis the joints become 
swollen and often suppurate, so that the articular surfaces become 
more or less destroyed. This may occur after infection during the 
puerperium or in any case of pyemia. Another arthritis, probably 
infectious, is sometimes seen in epidemic dysentery and in scarlet 
fever. Rarely immediately after, or some months after, typhoid 
fever a hypertrophic osteo-arthritis comes on as a result of a local 
disease produced by the baciUus of Eberth. This is to be separated 
from ordinary septic arthritis following typhoid fever. 

Acute Osteomyelitis. — The onset of an inflammation in the lower 
end of the femur or in the upper end of the tibia, producing what, at 
first glance, seems to be an arthritis and sometimes simultaneously 
involving other areas near joints, should raise a suspicion of acute 
osteomyelitis, which is a fatal disease in many cases unless surgical 
aid comes to the patient. The symptoms consist of boring pain in 



THE JOINTS 105 

the part, great tenderness and swelling, and the skin may break 
down as a purulent and offensive discharge makes its way to the 
surface. 

Closely allied to this is the acute epiphysitis of infancy, in which 
there is suddenly developed a chill followed by great pain and 
swelling of the joints or their neighborhood. The skin becomes 
engorged with the blood and the joint fills with pus. Care must 
be taken to separate this condition from rheumatism and the joint 
swelling sometimes seen after typhoid fever and that form which 
is due to infantile scurvy. 

Subperiosteal Hematoma. — Great swelling of the thigh or leg 
occurring in a child may be due to subperiosteal hematoma (Moller- 
Barlow's disease). Aspiration of the swelling will reveal the 
character of its contents, and the fact that the child is usually a 
sufferer from rickets will aid in the diagnosis. 

Gout. — Although gout is capable of causing deformity in the 
lower extremities, it has one fact about it which is of practical 
importance, namely, that it involves the small joints of the foot, 
while rheumatism attacks the large joints, such as the knee, by 
preference. Gout involves the feet more commonly, the big toe 
being the favorite place for gouty manifestation, whereas chronic 
rheumatism is more frequently seen in the hand, if small joints are 
affected. Aside from the swelling, redness, and exquisite tenderness 
of gouty joints, all of which symptoms exceed in acuteness, if pos- 
sible, similar manifestations in acute rheumatism, there is often an 
additional and permanent cause of deformity in the chalk stones 
which are deposited about the joints, and which are never seen in 
rheumatism. The history of frequently recurring attacks lasting 
but a few days, accompanied by enlargement of the veins about 
the joint and shedding of the skin locally, points, when added to 
the symptoms named, to a typical case of gout. In chronic cases 
it may be almost impossible to determine whether a case be one of 
chronic rheumatism or gout unless chalk deposits can be found. 
(See chapter on the Hand.) 

Sometimes in chronic lead poisoning we have developed what is 
known as plumbic gout, owing to the deposition about the joint of 
urate of lead and sodium. 

Dengue. — The onset of a multiple arthritis, with which there are 
headache, chills, intense aching in the bones, joints, and muscles, 
and a fever rising as high as 106 or 107 °, and rarely an erythematous 
rash, may indicate the presence of dengue. The joints are swollen 
and painful, and often both the large and small ones are involved. 

In Schbnlein's Disease, which is a form of very severe purpura, 
multiple arthritis, with great pain, and purpuric eruptions occur 
and the presence of the subcutaneous exudate with edema and 
sloughing of the mucous membrane of the mouth adds to the 



106 THE FEET AND LEGS 

picture. The patient seems very ill, but death rarely follows. Such 
cases are rare, but the writer saw one in consultation with Dr. 
Wilson, of Woodbury, New Jersey, in which alarming sloughs of 
the tonsils and buccal mucous membrane occurred in addition to 
the arthritic changes. (See chapter on the Skin.) 

Very nearly allied to this are the joint involvements of hemo- 
philia, which in their sudden onset and pain closely resemble rheu- 
matism, particularly as the large joints are commonly involved. 
The history of the patient being a bleeder, or of his being related 
to one, may clear up the diagnosis. 

Spontaneous Dislocation of the Hip. — So-called spontaneous 
dislocations of the hip have been recorded during convalescence 
from typhoid fever, scarlet fever, and acute rheumatism. The 
luxation in the latter disease usually follows severe pain, and the 
ligaments are often found torn from their attachments. In typhoid 
and scarlet fevers the dislocation occurs insidiously and announces 
itself by the pain and disability it causes. 

Periosteal Thickening. — Alterations in the appearance of the 
tibiae or shins often give us a clear. idea of the presence of late 
syphilis, either because of gummatous swellings in this neighbor- 
hood or owing to the development of periosteal thickening and 
exostoses. 

Intense Swelling. — Intense swelling of the leg, aside from that 
due to ordinary edema, may be due to thrombosis or milk leg, which 
is a condition of swelling of the entire limb, generally limited to 
one side, and seen during the puerperium or after any one of the 
infectious fevers, such as typhoid. The joints are not particularly 
affected. On the contrary, the calf of the leg is the part most 
affected, it being white, firm, hot, but slightly, if at all, edematous. 
Pain is excessive, there is entire loss of power in the affected limb, 
and its temperature is much higher than normal. 

If the swelling of the leg is bilateral and pits on pressure, it is 
practically always the result of anasarca from renal or cardiac dis- 
ease; but if unilateral, it may be, as just stated, due to thrombosis 
of the femoral vein. (See chapter on the Skin; Edema.) 

Gangrene. — Three very important and serious alterations in the 
nutrition of the foot remain to be noted, namely, perforating ulcer 
due to tabes dorsalis, diabetic gangrene, and senile gangrene. 

Perforating ulcer usually appears in one foot, beginning with the 
formation of a bleb, which changes to an abscess, which in turn is 
followed by necrosis of all the tissues of the foot immediately under- 
lying the destroyed skin. With it are associated the signs of ataxia. 
Sometimes perforating ulcer of the foot occurs during the course 
of diabetes mellitus, but it is probable in many such cases that 
locomotor ataxia is associated with diabetes. 

In diabetic gangrene the toes are nearly always affected in 



THE JOINTS 



I07 



preference to other parts of the body. An analysis of the urine 
will aid the diagnosis. (See chapter on the Skin.) 

In senile gangrene the age of the patient, the presence of bad 
bloodvessels, and the absence of a sufficient cause for gangrene, as, 
for example, trauma, separate the case from any other condition, 
while the additional facts that senile gangrene generally affects the 
inner side of the foot, especially the big toe, and is a dry gangrene, 
render the diagnosis easy. 




Fig. 28. — Testing the knee-jerk with the percussion hammer. 

Gangrene of the lower extremities sometimes follows the infectious 
diseases, such as scarlet and typhoid fevers, 1 from thrombosis of 
the femoral artery. It may also occur in the course of exophthalmic 
goitre. 

More rarely gangrene of the foot and hand follows embolism due 
to cardiac valvular disease. It is extremely painful, and septic 
fever may ensue. 

1 See "The Medical Complications and Sequelae of Typhoid Fever and Other 
Exanthemata, " by H. A. Hare and Beardslev. Lea Brothers & Co., Philadelphia, 
1909. 



io8 



THE FEET AND LEGS 



Mycetoma. — In this connection mention may be made of 
" Madura foot," or mycetoma, a chronic local disease of tropical 
climates, and called "fungus foot disease" in India. A smal] tumor 
develops on the foot or hand, which, after the lapse of twelve to 
twenty-four months, bursts and leaves several sinuses from which 
escape black particles or whitish-red bodies like fish-roe. The dis- 
ease may spread up the leg. The pale particles in the discharge 
look like actinomyces. 

Ainhum. — Ainhum is a disease peculiar to dark-skinned races, 
characterized by gradual drying up and separation of the toes (by 
a constriction), usually the little toe. It has been thought to be 
related to leprosy, but this is doubtful. 




Fig. 29. — Testing the knee-jerk by a blow with the ulnar edge of the hand. 



Physical Methods Employed in Examining the Feet and Legs. 
— The Knee-jerk. — The method of testing the knee-jerk consists in 
seating the patient on a chair of ordinary height, instructing him to 
cross his legs in the position which he would occupy if sitting at 



THE JOINTS 



109 



ease, and then to sharply tap the tendon of the knee-cap, between 
the patella and its insertion into the tibia, by means of a rubber 
hammer or with the ulnar edge of the hand. (See Figs. 28 and 29.) 




Fig. 30. — Testing the knee-jerk by means of the percussion hammer, the patient 

being recumbent. 




Fig. 31. — Testing ankle-clonus with the patient recumbent. 



no 



THE FEET AND LEGS 



When the patient is too weak to sit up, the lower limb may be 
elevated from the bed so that the thigh and leg are at an angle 
of about 45 degrees, the lower third of the thigh resting on the 
left hand of the physician in such a way that the leg hangs supine. 
(See Fig. 30.) 




32. — Testing ankle-clonus when the patient is seated. 



Ankle-clonus.— This test can be made when the patient is seated 
or recumbent. When recumbent the examiner grasps the leg near 
the knee with the left hand in order to support it. He then extends 
the leg on the thigh with the right hand, grasping the ball of the 
foot. When the limb is in this position, the leg being well extended 
on the thigh, the foot is flexed sharply toward the knee and 
immediately released from pressure. (See Fig. 31.) If clonus is 
present, the foot will undergo a series of coarse, tremulous move- 
ments in extension and flexion. 

Another method of testing clonus is to seat the patient in a chair 
with the leg resting on the ball of the foot on the floor, and then to 



THE JOINTS 



III 



apply sudden pressure, which is quickly relieved, to the knee, when, 
if clonus is present, the limb undergoes a series of tremulous 
up-and-down movements. (See Fig. 32.) 




Fig. 33 — Testing the "station." Eyes closed; feet close together. 

Station. — This is determined by having the patient stand with 
his feet close together and then directing him to close his eyes, or if 
he cannot be relied upon to completely close his eyes, to blindfold 
him. (See Fig. 33.) A normal patient should stand almost per- 
fectly steadily under these circumstances, but in several diseases, 
notably locomotor ataxia, he will sway very greatly, or even fall. 

The Cremasteric Reflex.— This reflex consists in a retraction of 
the testicle and scrotum upon irritating the skin upon the inner 
surface of the thigh. (For methods of testing the various conditions 
of sensibility in a limb, see chapter on the Skin.) 



CHAPTER IV. 
HEMIPLEGIA. 

Having considered the manifestations of disease as seen in the 
arms and legs in connection with monoplegia and paraplegia, spasm 
and contracture, we may now study the diagnostic meaning of 
hemiplegia, or that form of paralysis which involves the arm and 
leg and head on one side of the body. This form of paralysis, when 
complete, is always due to a lesion arising above the spinal cord — 
that is, in the brain, and is due to lesions in the lower tracts of the 
brain or in its cortex. The character of the paralysis, the associa- 
tion of other symptoms with it, and the history of the patient and 
of his illness, will render a diagnosis easy as to the approximate 
site of the lesion in most cases. The most common causes are 
hemorrhage into the cerebral tissues from a ruptured bloodvessel, 
or embolism or thrombosis of some vessel supplying important 
areas. Still other causes of hemiplegia are brain tumors, meningeal 
hemorrhage, degenerative processes, and hysteria. 

Before entering into a consideration of the various symptoms 
resulting from central nervous lesions it is well to stop for a moment 
for the purpose of clearly understanding the anatomy and physiology 
of the parts involved, in order that we can properly study the 
results of lesions in the nerve centres or nervous tracts. 

It is not necessary to remind the reader that the brain is divided 
into three areas, the frontal area being concerned with intellection, 
the middle area with motion, and the posterior area with sensation 
and special sense. These areas are again divided into subareas, 
each of which governs or is connected with several functions, and 
still further subdivisions exist, in which reside the centres governing 
small areas, as, for example, a single muscle or group of muscles. 
(See Fig. 34.) Disease of any part of the brain surface, therefore, 
modifies more or less the function of that part and the part of the 
body tributary to it. Beneath the surface, through the so-called 
white matter, various fibres pass, which carry to or from the 
centres in the cerebral cortex the impulses connected with their 
function, and these fibres approximate one another more and more 
closely in the lower part of the brain until they form a bundle (the 
corona radiata). Thus we see in Fig. 34 how the fibres arising from 
the middle area of the cortex cerebri pass down between the 
caudate and lenticular nuclei and the optic thalmus into the 



HEMIPLEGIA 



113 




Fig. 34. — Diagram showing the fibres from the cortex forming the corona 
radiata, which after they are approximated pass into the internal capsule. It 
also shows the decussation of the pyramid of the left side, which passes to the 
right side of the spinal cord, and the direct or uncrossed tract (Tiirck's column). 
Finally it also shows the secondary degeneration which occurs after cerebral 
hemorrhage or softening, and which follows the course of the motor tracts into 
the spinal cord. H, site of lesion. The continuous lines are fibres going to the 
legs, the dotted are those going to the arms and motor cranial nerves. (Modified 
from Van Gehuchten.) 



ii4 



HEMIPLEGIA 



knee or angle of what is called the internal capsule. These 
fibres are arranged in such a way that those arising from the 
lower part of the cortex, as in the face centre, lie nearest the 
knee of the capsule, and those highest, farthest from this 




Fig. 35. — Cross-section of the brain, showing the lateral ventricles, the cere- 
bellum, and, most important, the cross-section of the motor fibres in the internal 
capsule shown on one side. (Modified from Fuller.) 

point (Fig. 35). After the motor fibres have passed through the 
internal capsule they pass into the crus cerebri of that side, 
which (the crus cerebri) connects the hemisphere of the same side 
with the cerebellum behind it, and the pons and medulla below it. 



PLATE II 




Base of the Brain, showing the Cranial Nerves. 

The crura cerebri are seen on either side of the posterior perforated space and under the 
third nerves. The various cranial nerves are numbered with Roman numerals. (Modified from 
Arnold.) 



HEMIPLEGIA 



II 



The crura cerebri are two thick, cylindrical bundles of white matter 
which emerge from the anterior border of the pons (see Plate II), 
diverge as they pass upward and outward to enter the under part of 
each hemisphere, as if stretching out to receive the motor fibres from 
the internal capsule. From the crura cerebri the motor fibres pass 



Lesion of cerebral mo- 
n opleg ia (brack ia I ) 



Lesion of ordinary 
hemiplegia 



Lesion of cross paralysis 
(face of same side with 
limbs of other side) 



A lesion causing paraplegia 



A lesion causing hemi- 
paraplegia 




Cortical centre for op- 
posite leg 



Cortical centre for op- 
posite arm 



Cortical centre for op- 
posite side of face 



Internal capsule (pos- 
terior limb) 



Motor nerve to face 



Decussation of pyra- 
mids 



Crossed pyramidal tract 



Motor nerves to upper 
limb 



Crossed pyramidal tract 



Sensory nerves entering 
cord, and decussating 
soon after entry 



Motor nerves to lower 
limb 



Fig. 



36. — Diagram showing the general arrangement of the motor tract and the 
effect of lesions at various points. (Ormerod.) 



downward into the pons Varolii. Here the fibres which have 
hitherto travelled together divide into two parts, namely, those 
from face and tongue centre, which pass to the opposite side and 
become connected with the nuclei of the facial and hypoglossal 
nerves, which act as minor centres governing the face and tongue, 
and the fibres for the arm, leg, and trunk of the body, which 
continue on down to the medulla oblongata, where they form the 



n6 



HEMIPLEGIA 



so-called pyramids, and having done so most of the fibres cross to 
the opposite side of the spinal cord (the crossing of the pyramids) , 
and so form the crossed or lateral pyramidal tracts. (See Fig. 
34.) A smaller number of fibres, however, pass directly down to 
the spinal cord from the medulla oblongata, and form what is 




Fig. 37. — Showing the mechanism of different hemiplegias. A lesion at A 
causes complete hemiplegia by destroying the motor tract. One at M causes 
paralysis of third cranial nerve (motor oculi) by destro3 T ing its nucleus or root on 
same side, and paralysis of arm and leg on opposite side. A lesion at F causes 
facial palsy on same side, hemiplegia on opposite side. In a lesion at H the 
hypoglossus would be affected on one side, with hemiplegia on the other. (Modi- 
fied from Edinger.) 



called the direct or anterior pyramidal tract. Direct, because it 
does not cross; anterior, because it lies along the edge of the anterior 
fissure of the cord; pyramidal, because it comes down from the 
pyramid. This is sometimes called Tiirck's column. (See Fig. 34.) 
It is by means of these two tracts in the spinal cord that motor 
impulses pass down to the nerve trunks and muscles. 

We can understand, therefore, that if a small lesion occurs at the 
peripheral endings of the corona radiata — that is, on the cerebral 



HEMIPLEGIA 



117 



cortex — it will only produce a limited paralysis. Thus, as seen in 
Fig. 34, a clot at the arm centre would only involve the arm fibres. 
If, however, the lesion be lower down where the fibres of the corona 
radiata are getting closer and closer, as, for example, in the internal 
capsule, then even a small lesion will produce widespread paralysis 
since it will involve a large number of fibres running ultimately to 
widely separated areas in the body, and, if large enough, produce 
hemiplegia. (See Fig. 34, lesion H, and Fig. 37, lesion A.) If the 
lesion be situated in the pons on one side, it will cause facial par- 
alysis on that side and hemiplegia on the opposite side of the body, 
because, as shown in the diagrams (Figs. 36 and 37, M), it will, 
under these circumstances, destroy the facial fibres after they have 
crossed, and the remaining motor fibres before they cross. The 
various tracts, motor and sensory, in the spinal cord are shown in 
Fig. 38. 




Fig. 38. — Showing the various tracts in the spinal cord on cross-section. 
(Nervous Diseases, Mills.) 



Hemiplegia from Hemorrhage is characterized by sudden onset 
in most cases, by more or less mental disturbance and disorders of 
motion, sensation, and of the special senses according to the site 
of the leaking vessel. The skin reflexes are apt to be markedly 
decreased and the deep reflexes increased, but the bladder and 
rectum are not usually paralyzed, although in the first shock of the 
accident there may be vesical and rectal incontinence. The mental 
disturbance usually amounts to a rapidly oncoming unconsciousness 
in hemorrhagic hemiplegia. 



Il8 HEMIPLEGIA 

The question of the location of the lesion is very important. In 
the great majority of cases it is situated above the point at which 
the decussation of the motor fibres takes place in the medulla, 
and is, therefore, on the opposite side of the body from that on 
which the hemiplegia exists. If, however, the lesion be below the 
decussation, the paralysis and lesion are on the same side, as just 
described. 

The most common site for the lesion in hemiplegia is in the 
knee or posterior limb of the internal capsule, owing to the fact that 
the middle cerebral artery in one of its lenticulostriate branches 
perforates the internal capsule, and ends in the caudate nucleus, 
and this artery is so commonly ruptured that Charcot has called it 
the "artery of cerebral hemorrhage" (Fig. 39). If the hemorrhage 
does not involve the posterior third of the internal capsule, there 




Mid. C 



Fig. 39. — Showing distribution of bloodvessels to internal capsule. The 
artery marked x is the so-called artery of cerebral hemorrhage, and it is readily 
seen how its rupture destroys the fibres in the internal capsule. (Modified from 
Gordinier.) 

are no sensory symptoms associated with the motor loss, but the 
paralysis will be practically universal on that side, involving the 
leg and arm,, and the lower part of the face, so that the mouth is 
drawn toward the healthy side. (Explained by Fig. 35.) The 
symptoms associated with hemiplegia due to this cause often become 
very severe, because the hemorrhage is so profuse that the lateral 
ventricle becomes rilled with blood, and from it the blood passes to 
the third and from there to the fourth ventricle, where, by pressure 
on the vital centres, it speedily produces death. In such cases deep 
unconsciousness, stertorous breathing, a slow, full pulse, and a 
flushed skin, becoming somewhat cyanotic, may be present. Re- 
covery never occurs, for the secondary inflammation, or softening, 
following the outflow of blood produces fatal results, even if the 
patient survives for some days. 

In cases in which the hemorrhage is very limited consciousness 



HEMIPLEGIA FROM HEMORRHAGE 119 

may be lost for only a brief period, and at most there may be only 
mental confusion. Often in mild cases there is a slight return of 
power in the affected side within a few days, and the temperature 
of the affected part, which has been raised, approaches the normal. 
Finally, after six to eight weeks, the dominant symptoms consist in 
partial loss of power of the arm and leg, and the facial paralysis 
has perhaps entirely disappeared, although the tongue when pro- 
truded may tend to go over to one side. If the case does not pass 
to such favorable results, instead of recovery of power at this time 
there are developed contractures and secondary rigidity from degen- 
erative processes extending to the pyramidal tracts. (See Fig. 34.) 
Hitzig has shown that these conditions are apt to be least marked 
in the morning. Wasting of the paralyzed muscles ensues only 
from the disuse and not from true trophic change, and the electrical 
reactions would be normal. 

When the case is not of the very severe type which causes death 
in a few hours, and yet the lesions are such that recovery is not 
going to take place, the -patient at the third or fourth day becomes 
unconscious a second time, his temperature rises, he mutters, and 
grows restless, finally becomes comatose, then develops respiratory 
failure, or a hypostatic congestion of the lungs, and dies. 

When a patient is seized with headache, dizziness, vertigo, and 
vomiting, and rapidly oncoming hemiplegia and hemianesthesia, 
attended at first with no loss of consciousness, but in a day by un- 
consciousness and coma, he is suffering from what has been called 
"ingravescent apoplexy." The hemorrhage, under these circum- 
stances, begins in the knee of the internal capsule, proceeds back- 
ward until it involves the sensory fibres in the internal capsule, 
and, finally, breaks into the lateral ventricle, soon after which death 
ensues. 

When a hemiplegia is followed by rigidity very early, with sen- 
sory involvement and convulsions, the lesion is probably cortical, 
or, more correctly, is secondarily cortical to a deeper hemorrhage, 
and spreads over the centres for the face, arm, and leg. Most 
commonly, cortical hemorrhages are due to injuries, although they 
may arise from unprovoked vascular rupture. In any case, they 
are usually ushered in by convulsions. (See page 120.) 

If in the development of symptoms of cerebral hemorrhage there 
be little hemiplegia and temporary unconsciousness, followed in 
some hours by a sudden aggravation of the symptoms, it may be 
that in the beginning of the attack the lesion has been in the frontal 
lobes, but has gradually extended backward until it has ruptured 
into the lateral ventricle. So, too, a hemorrhage into the occipital 
lobe or the posterior part of the parietal lobe is rarely marked by 
much hemiplegia, and, if present, the leg is more paralyzed than the 
arm. A characteristic symptom of this lesion is, however, well- 



120 HEMIPLEGIA 

marked hemianesthesia (see chapter on the Skin) and hemianopsia 
(see chapter on the Eye). Generally, however, such changes 
result from a thrombosis. 

Hemiplegia developing after an injury to the head is usually due 
to rupture of the middle meningeal artery or one of its branches. 
(See Plates III and IV.) Owing to the fracture of the skull, the 
vessel is ruptured. A pathognomonic sign of this accident is the 
fact that there is a period of consciousness between the time of 
injury and the development of unconsciousness. The patient may 
be momentarily stunned, then recover consciousness, and then 
relapse into a second period of unconsciousness which rapidly 
deepens into profound coma. It is important to remember that 
while the paralysis is on the opposite side of the body from the 
hemorrhage, the hemorrhage may be on the opposite side from the 
external injury, since the fracture of the skull may be a fracture by 
contrecoup. The paralysis is usually progressive from part to part, 
and convulsions may occur as a result of cortical irritation produced 
by the hemorrhage. A wide dilatation of the pupil on the side of 
the hemorrhage ("Hutchinson's pupil") may be present. Such a 
hemorrhage is said to be supradural. Sometimes the hemorrhage 
arises from the ascending frontal or ascending parietal artery, and 
is then subdural. 

The following table, from Mills' Nervous Diseases, gives the 
differentiation between ventricular and meningeal bleeding: 

Ventricular Hemorrhage. Meningeal Hemorrhage. 

No antecedents to explain the lesion. Antecedents : for the newborn a pro- 

longed or hard labor ; for the adult a 
traumatism. 
Premonitory symptoms not rare. Premonitory symptoms generally absent. 

Gradually deepening unconsciousness. When traumatic, unconsciousness fol- 

lowed by partial restoration of con- 
sciousness and then again by uncon- 
sciousness. 
Cephalalgia rare. Cephalalgia frequent. 

Paralysis when present is usually hemi- Paralysis ordinarily generalized ; hemi- 

plegic. plegia exceptional. 

Varying pupillary conditions. Unilateral dilatation of pupil common. 

Deviation of the mouth and tongue very Deviation of the mouth and tongue rare. 

common. 
Contractures very common. Contractures, although frequent, less 

common. 
Convulsions may be present, but not Convulsions the rule. 

common. 
Vomiting not frequent. Vomiting frequent. 

No symptoms of secondary meningitis Symptoms of secondary meningitis with 
with fever. high fever toward the third or fourth 

day. 
Death rapid. Life, as a rule, prolonged several days. 



PLATE III 




~~r**. 



Showing the Area of the Middle Meningeal Artery, in the Inner Table of the 
Skull, Injury to which is Sometimes the Cause of Hemiplegia. (Arnold's Atlas.) 



PLATE IV 




The same Artery with the Inner Table of the Skull Removed. (Arnold's Atlas.) 



EMBOLISM AND THROMBOSIS 121 

When there is developed in cases of hemiplegia, aphasia or dis- 
ordered speech, there is probably a lesion in the neighborhood of 
the third frontal convolution, or the island of Reil. (See chapter 
on Speech.) 

Hemiplegia may be due to cerebellar hemorrhage, in which case 
there are loss of consciousness deepening into profound coma, con- 
tracted pupils, vomiting in many of the cases, and finally death 
when the hemorrhage breaks into the lateral ventricle. The 
diagnosis of cerebellar hemorrhage is very difficult. 

Of the irregular forms of hemiplegia there are several. Some- 
times the leg is from the beginning more affected than the arm, and 
remains paralyzed long after the face and arm has recovered. The 
leg may become rigid and distorted by contractures, and there will 
often be found present marked anesthesia of the skin of the para- 
lyzed leg and arm, with hemianopsia and aphasia. Such symptoms 
indicate a lesion of comparatively small size involving the leg 
fibres and some of the sensory fibres in the internal capsule, and 
result from rupture of the lenticulo-optic artery. When the arm 
suffers most the symptoms just described as occurring in the leg 
are found in it, and motor aphasia, if the lesion is on the left side, 
is often very marked, as is also facial paralysis. This is supposed 
to be due to the anterior frontal artery, a branch of the inferior 
anterior cerebral artery, becoming diseased. 

When posthemiplegic chorea attacks the paralyzed limbs there is 
often a focal lesion in the posterior extremity of the internal capsule. 

Embolism and Thrombosis. — The symptoms which have just 
been detailed may also arise, as already said, from embolism or 
thrombosis of the cerebral vessels. How are we to separate the 
hemiplegias of hemorrhage and occlusion? In many cases this 
is impossible, but there are some differential points which may 
aid us. In the first place, thrombosis is a condition of advanced 
age, while hemorrhage may occur at any time from thirty years of 
age on. The presence of hemiplegia in a young man, therefore, 
is probably not due to a thrombosis, unless of syphilitic origin. 
Again, hemorrhage occurs often after exertion or the drinking of 
stimulants, and occurs rarely in sleep, whereas thrombosis not rarely 
comes on under these circumstances, and often develops during the 
night, so that the patient awakes paralyzed, but a patient may have 
both thrombosis and apoplexy. In hemorrhage, consciousness is gen- 
erally lost, whereas in thrombosis it is often only dimmed. Vomiting 
and contracted pupils from pressure on the lower centres indicate 
hemorrhage, while their absence may point to thrombosis. Finally 
the general systemic shock and febrile movement are apt to be 
greater in hemorrhage than in thrombosis. The history of syphi- 
litic infection, producing an endarteritis, also points to thrombosis, 
although hemorrhage may arise from this cause also. 



122 HEMIPLEGIA 

The diagnosis of embolism producing hemiplegia from the par- 
alysis due to hemorrhage is always more or less difficult, but the 
presence of chronic or ulcerative endocarditis or their results, or 
other cause for the formation of emboli, aids the diagnosis. Where 
the cause is embolism the onset is sudden, whereas in thrombosis 
it is sometimes more gradual. The paralysis from embolism is more 
commonly on the right side of the body, owing to the fact that it 
is more easy for an embolus to pass into the left middle cerebral 
artery than into the right. 

Additional Causes of Hemiplegia. — Spastic hemiplegia may be 
due to cerebral tumor, and is often associated with convulsions, 
particularly if the growth be cortical. Very often the paralysis of 
cerebral tumor will be found, from the history, to have come on 
gradually. Thus, the history may be that at first the side of the 
face has been paralyzed, then the arm and then the leg, and that 
the complete loss of power has not been sudden but gradual in the 
part affected, or that a convulsion has left that side, which was 
previously only impaired in strength, totally paralyzed. 

Hemiplegia also comes on as a result of cerebral syphilis, and, 
aside from a history of specific infection and response to specific 
medication, presents few characteristic signs. The presence of 
intense headache, convulsions of an epileptiform type, and the fact 
that the paralysis occurs in some cases in early adult life, point to 
its origin. A positive Wassermann test would be also suggestive. 

Another cause of hemiplegia is diffuse cerebral sclerosis of one 
hemisphere (net multiple sclerosis), in which the most constant 
symptoms are, in addition to the paralysis, evidences of motor 
irritation, such as epileptoid convulsions of a bilateral or unilateral 
character, rhythmical or arrhythmical twitchings of the muscles 
like chorea, and dementia. 

Hemiplegia arising from acute infantile cerebral paralysis has 
many of the distinctive features already described when discussing 
the paraplegia due to this diseased state. The age of the patient, 
the occurrence of epileptiform convulsions and of athetosis in the 
affected parts, and the patient's history are the important points to 
be recalled in making a diagnosis. The lesion is always due to a 
cerebral hemorrhage or to embolic softening. 

When hemiplegia occurs in locomotor ataxia, it depends not upon 
the disease, but upon a complicating hemorrhage, embolism, or 
thrombosis. 

A slowly developed hemiplegia sometimes results from dissemi- 
nated sclerosis, the pathological process involving the side of the 
pons and spinal cord, but the intention tremor, the peculiar speech, 
the nystagmus, and the very excessive reflexes aid us in the diag- 
nosis of the cause of the loss of power. (See chapter on the Hands 
and Arms, part on Tremor.) 



CROSSED PARALYSIS 1 23 

A form of hemiplegia which is often very misleading is that 
occurring in general paralysis of the insane or paretic dementia. In 
this disease the patient often has attacks of vertigo, unconscious- 
ness, and more or less marked hemiplegia or monoplegia, sometimes 
with aphasia if the right side is paralyzed. This form is also liable 
to be wrongly diagnosticated by reason of the epileptiform convul- 
sions, which frequently occur, and which in connection with the 
paralysis give the impression in the first attack that there is a 
hemorrhage of the cerebral cortex. The altered disposition of the 
patient, the loss of memory and intelligence, the peculiar stumbling 
speech, and the curious changes in the handwriting are some of the 
symptoms which complete the diagnostic picture. The paralysis, 
moreover, is usually transient in character. 

In this condition we should not forget the possibility of hemiplegia 
or monoplegia occurring with suddenness in the course of renal 
disease producing uremia. The paralysis may be permanent or 
only transient, but the urine will be found to be albuminous, and 
the other signs of renal disorder may be manifest. 

Hemiplegia sometimes comes on in purulent meningitis. The 
history of a head injury or of a pyemic or infective process, the 
cerebral symptoms, the stiffness of the back of the neck, the impair- 
ment of the normal movements of the eyeball, and the optic neuritis, 
associated with the convulsions, make the diagnosis possible. 

Crossed Paralysis. — -When there is paralysis of the arm, trunk, 
and leg on one side, with facial paralysis and anesthesia on the 
opposite side of a well-marked type, associated with early rigidity 
of the paralyzed side, conjugate deviation of the eyeballs, a very 
marked rise in bodily temperature, a contracted pupil, and con- 
vulsions, with difficulty in swallowing and in speech, the lesion is 
to be found in the pons Varolii on the side opposite the paralysis. 
This is due to the fact that the injury is below the decussation of 
the facial nerve. (See Fig. 36.) If both sides of the face are 
paralyzed, with hemiplegia elsewhere, the lesion is in the pons 
where the facial fibres cross. Pons paralysis is nearly always 
associated with giddiness, vomiting, conjugate spasm with nystag- 
mus, albuminuria, glycosuria, and marked disturbances in the 
respiration and heart. Pontile hemorrhages are, however, very 
rare, and usually are rapidly fatal. 

If in a case of hemiplegia there is not only paralysis of the arm 
and leg and of the lower part of the face in one side, but in addition 
paralysis of the upper part of the face on the opposite side with 
ptosis on that side due to paralysis of the facial and oculomotor 
nerves, and with these symptoms impaired sensibility and vaso- 
motor changes in the limbs, the lesion is probably in the cms 
cerebri on the side of the upper facial paralysis — that is, on the same 
side as the ptosis. This is only true if the two paralyses have been 



124 HEMIPLEGIA 

simultaneous in occurrence, as it is possible for two lesions occurring 
at different times and at different places to produce paralysis of the 
face on one occasion and hemiplegia on another. (See Ptosis in 
chapters on the Face and the Eye.) 

A very rare form of paralysis, in which the arm on one side and 
the leg on the other side are involved, is due to a bulbar lesion just 
where the decussation of the pyramids takes place. This is one of 
the forms of crossed paralysis, and is due to cutting off of one set of 
fibres before they cross, and the others after they have crossed. 
(See early part of this chapter and chapters on the Hand and Arms, 
Feet and Legs, and Face and Head, for further information as to 
crossed paralysis.) 



CHAPTER V. 



SPEECH. 



The changes in the speech and voice — Their significance — Aphasia— Apraxia — ■ 

Alexia — Paraphasia . 

The character of the speech and the tones of the voice often 
convey a considerable amount of diagnostic information to the 
physician. While in many diseases no marked alterations to the 
normal manner of speech are present, in others marked changes 
take place. Thus in acute laryngitis due to exposure to cold or 
irritant vapors the patient has a whispering voice. In persons 
suffering from pulmonary tuberculosis the development of hoarse- 
ness and whispering or labored speech tells us only too well of the 
fact that the grave and distressing complication called laryngeal 
tuberculosis has arisen, and that the progress of the case will be 
more rapid toward the fatal result. Again, the sudden onset of 
whispering voice or complete aphonia occurring in a young girl 
whose facies is hysterical, should always arouse a suspicion of 
hysteria, while if the signs of this condition are absent and the 
patient has none of the signs of tuberculosis, we should examine 
the larynx for a papillomatous growth. Again, if hoarseness or a 
whispering voice is manifested by a male of adult years, who is 
also suffering from dyspnea, unilateral flushing or sweating of the 
face and neck, and unequal, rapid radial pulses, we should suspect 
aortic aneurysm or a mediastinal tumor which is pressing on his 
recurrent laryngeal nerve. There are also other causes of hoarse- 
ness due to nervous lesions arising from the long and tortuous 
course of the nerves supplying it. These have been well grouped 
together by Felix Semon. (See Table on page 126.) It is inter- 
esting to note that in suspected cases of disease of the parts herein 
named it is well to make a laryngeal examination, since this may 
reveal a paralyzed cord, although the voice has not indicated such 
a condition, because by great retraction of the opposite cord the 
laryngeal opening is kept patulous and phonation is possible. 

Hysterical mutism may occur in both males and females. It 
usually follows a fright or violent emotion, or it ma}' follow an 
hysterical seizure. Sometimes it develops without any such 
history. The condition lasts from a few hours to months or years. 
and recovery is often as. sudden and unsuspected as the onset. As 



126 



SPEECH 



a rule, the tongue, lips, and jaws are unimpaired in their functions. 
Sometimes, however, these parts are affected by hysterical spasm. 
Often there will be hysterical anesthesia with the mutism. (See 
chapter on Skin.) Usually there is no evidence of cerebral lesion 
in such cases in the sense of impairment of intellect. 



Table Showing the Possible Causes of Laryngeal Paralysis. 



I. Bulbar and Bulbospinal Affections. 

1. Hemorrhage and softening. 

2. Syphilitic processes. 

3. Tumors. 

4. Diphtheria. 



5. Progressive bulbar paralysis. 

6. That curious form of systemic central 
nervous disease first described by Hughlings 
Jackson and Morell Mackenzie, in which one- 
half of the tongue, the corresponding half of 
the palate, the corresponding vocal cord, 
and, in a number of cases, the corresponding 
trapezius and sterno mastoid muscles are 
affected. 

7. Amyotrophic lateral sclerosis. 

8 Disseminated cerebro-spinal sclerosis. 
9. Syringomyelia. 
10. Tabes dorsalis. 



II. Peripheral Affections. 

1. Acute rheumatic influences. 

2. Catarrhal neuritis. 

3. Toxic influences (lead, arsenic, etc.). 

4. Tumors in the posterior cavity of the 
skull or in the foramen lacerum or foramen 
jugulare. 

5. Pachymeningitis. 

6. Traumatism (unintentional ligature of 
nerves, injection of iodine into a goitre, cut 
throat, stabbing, injury during extirpation of 
goitre, etc.). 



7. Tumors of neck (goitre, peritracheal 
glands, etc.). 

8. Aneurisms of the arch of the aorta, In- 
nominate, subclavian, carotid. 

9. Mediastinal tumors malignant, tubercu- 
lous, calcification of bronchial glands, etc.). 

10. Pericarditis. 

11. Pleurisy. 

12. Tuberculosis and pleuritic thickening of 
apex of right lung. 

13. Chronic pulmonary affections (chronic 
pneumonia, anthracosis, etc.). 

14 Infectious fevers (typhoid, etc.). 
15. OT>ophagenl carcinoma. 



When a child speaks with a nasal twang or indistinctly we suspect 
the presence of adenoid vegetations, and will probably find that he 
or she is addicted to mouth breathing. Stuttering or stammering 
may also be due to this cause. 

A feeble, hesitating speech is often a sign of exhausting disease, 
and a short and quick but feebly spoken sentence generally indicates 
that the patient is suffering from some cardiac or pulmonary com- 
plaint, which renders him short of breath, so that he hurries through 
the sentence in order to be able to breathe freely again. In cases of 
pneumonia or of pulmonary edema this hurried speech is a very 
characteristic sign. 

Again, in cases of typhoid fever, when the tongue is dry and 
immobile from accumulated sordes, a mumbling character of the 
speech is present, even when the intellect is entirely clear, and in 
severe stomatitis the same quality of the voice may be present. 



APHASIA 127 

It is in connection with the disorders of the nervous system, how- 
ever, that the most typical alterations of the voice occur. Let us 
suppose that a patient from twenty to forty years of age develops 
a slow, scanning speech, with intention tremors (see chapter on 
the Hands), nystagmus, and more or less muscular weakness. In 
all probability he is a sufferer from insular or, as it is otherwise 
called, disseminated sclerosis. When he speaks each syllable is 
sharply accentuated and slowly pronounced. The only other 
condition in which a slow, scanning speech is of great diagnostic 
importance is in that rare disease Friedreich's ataxia; but the facts 
that this disease begins in childhood, that several members of the 
family are apt to be affected, that there are ataxic symptoms and 
early talipes equinus, render it easy to separate this affection from 
insular sclerosis. (See Paraplegia, in chapter on the Feet and Legs.) 

A hesitating, halting speech associated with Argyll-Robertson 
pupils, unequal pupils, mental deterioration, delusions, emotional 
or depressive, and tremor of the tongue, which last symptom may 
be so marked as to cause the speech to be indistinct and blurred, 
is indicative of paretic dementia. 

If an incoherent speech develops in a child who is not suffering 
from an acute illness causing delirium, there will usually be found 
in association with this symptom the nervous twitchings of chorea, 
for speech disturbances occur in about one-third of the patients 
suffering from this disease. 

A very indistinct speech of a mumbling character, great difficulty 
being experienced in the pronouncing of dental and lingual sounds, 
and perhaps associated with feebleness of the voice, if the larynx 
is involved, is seen in cases of glossolabiopharyngeal paralysis. If 
the cause of the defective speech be this disease there will be found, 
as associated symptoms, wasting of the tongue, Ungual tremors, 
some dribbling of saliva from the mouth, and immobility of the 
lips, the face about the mouth being expressionless. 

Somewhat similar symptoms due to paralysis of the lips, with 
escape of the tongue and pharynx, at least for a long time after 
labial paralysis develops, are sometimes seen in advanced cases of 
amyotrophic lateral sclerosis; and a still more close resemblance 
may be produced by the so-called " pseudobulbar paralysis," the 
lesion of which is in the motor cortex of the brain on both sides, in 
the lower part of the ascending frontal convolution. Rarely the 
latter is only a unilateral disease. 

A rather shrill, piping voice, the sentence being begun with hesi- 
tation and then hurried to an end in a rapid volley of words, is 
sometimes seen in paralysis agitans. 

Aphasia. — By far the most interesting speech defect is that 
called aphasia. It is divided into motor aphasia and sensory 
aphasia. 



128 SPEECH 

Before studying these conditions we must discuss the nervous 
mechanism of speech. When a child learns to talk it performs a 
purely imitative act. Its auditory nerve conveys the sound to its 
perceptive centres, and from here an impulse is sent to its motor 
speech centres, and these again send impulses to the inferior speech 
nuclei in the medulla oblongata, which in turn move the muscles of 
speech. Simultaneously the child learns the words and stores them 
in memory centres for sounds, and also stores in memory centres 
" motor memories," which tell him how to repeat the muscular 
movements a second time. Again, when he learns to recognize 
objects and call them by name he must use " visual memory" 
centres. These centres are all best developed in the left hemi- 
sphere of the brain in right-handed persons and in the right half 
of the brain in left-handed persons. 

If a person suffers from pure aphasia, he simply loses the memory 
of how to say certain words, and the lesion is in the third left frontal 
(Broca's convolution). This state is sometimes called aphemia. 
The patient knows what a knife is when he sees it, but he cannot 
recall his motor memories so as to move the muscles to say "knife." 
He can read to himself, because he has not forgotten the meaning 
of the words, and for this reason he understands what is said to him, 
and may be able to repeat a word immediately after it is said, by 
a purely imitative process. Generally, we find with aphasia a 
condition called agraphia, in which the patient cannot write his 
thoughts, but can copy perfectly. In the great majority of cases of 
aphasia, however, the patient is paralyzed in his right hand, so that 
the symptoms of agraphia cannot be demonstrated. Under the 
name of paraphasia we sometimes meet with a condition in which 
the patient can speak quite freely, but transposes words or inter- 
polates useless words to such an extent that what he says is un- 
intelligible. When the patient slips words, the lesion is in the 
associating tracts between the speech centres, and this is called 
conduction aphasia. 

In another condition closely connected with aphasia we have a 
state in which the patient can spell out words from a page set before 
him, but he cannot read, because the words convey no idea to him. 
This is called alexia, or "word blindness." Again, he may forget 
the use or significance of certain objects, such as a knife and fork; 
this is called apraxia. Still further, words when spoken to the 
patient in his native language may be heard perfectly, and yet 
understood no more than if in some unheard-of language. This is 
called "word deafness." 

If the patient has simple aphasia he has a lesion in the third 
frontal convolution in its posterior part. If he has word blindness 
or alexia, the lesion is in the angular gyrus, extending back into 
the occipital convolution. If he has apraxia or the loss of memory 



APHASIA I29 

of objects, the lesion is in the same area as in alexia; and if "word 
deafness" is present, the lesion is in the posterior part of the first 
temporal and upper' part of the second temporal convolution of the 
left hemisphere. As the various symptoms of aphasia in all its 
forms are closely associated with those of focal lesions of the brain, 
resulting, for example, from hemorrhage or embolism, the reader 
should read the chapter on Hemiplegia in this connection. 

Aphasia is quite frequently met with as a symptom of hysteria, 
and may occur independently of any organic lesion, so far as we 
know, in children during convalescence from an attack of a severe 
infectious disease. In the latter cases speech may return many 
months after. 

It is not to be forgotten that speechlessness is often present in 
melancholia and dementia. Further, temporary speechlessness or 
apparent aphasia may follow severe typhoid fever as a result of cor- 
tical exhaustion without the development of hemorrhage, embolus, 
or thrombus. The prognosis of this latter form is favorable. 

The following plan of testing a patient, devised by Eskridge 
from a shorter one by M. Allen Starr, may be followed with 
advantage : 

1. The power to recognize objects seen, heard, felt, tasted, 
smelt, and their uses. 

2. The power to recall the spoken names of objects seen, heard, 
felt, tasted, and smelt. 

3. The power to understand sounds other than speech. 

4. The power to understand speech and music. 

5. The power to call to mind objects named and point them out 
at request. 

6. If word-deaf, can he recognize his own name when it is 
spoken? 

7. The power to recognize a word spelled aloud. 

8. The power to call up mentally the sound of a note, figure, 
letter, or word. 

(The examination thus far will test the various sensory areas, but 
more especially the auditory and the association tracts between the 
different sensory areas connected with speech.) 

9. The power to recognize letters, figures, notes, and colors 
seen. 

10. The power to understand printed and written words seen. 

11. The power to read printing, writing, and music aloud and 
inaudibly, and to understand what he reads. 

12. The power to recall objects the names of which are seen. 

13. The power to write voluntarily. 

14. The power to write at dictation. 

15. The power to copy, and the manner of copying, printing. 
and writing. 

9 



130 SPEECH 

16. The power to write the names of objects seen, heard, felt, 
tasted, and smelt. 

17. The power to read aloud and inaudibly, and to understand 
what has been written. 

18. The power to write his name and the ability to read it when 
written by himself and by another person, or when it is printed. 

19. The power to recognize a letter by tracing it with the index 
finger or with a pencil, the movements being guided by another. 

20. The power to call up mentally the appearance of an object, 
a figure, a note, letter, or word, when word-blind. 

(These additional tests will aid in determining the condition of the 
visual word memories in the angular gyrus, and the connection 
between this area and the surrounding sensory and motor areas.) 

21. The power to speak voluntarily, and, if impaired or lost, the 
character of the defect. 

22. The power to repeat words after another. 

23. Does the patient recognize his mistakes in speaking and 
writing, and can he correct them? 

24. Can the patient think in speech (propositionize) ? 

25. Is there any special difficulty in the use of nouns, verbs, or 
other parts of speech? 

26. The power to understand pantomime or gesture expression. 

27. The power to employ intelligently gesture in expression. 

28. The power to read figures and to calculate. 

29. The power to count both money and in numbers. 

30. The power to play a game of cards or other games. 



CHAPTER VI. 
THE SKIN. 

The color of the skin — Eruptions on the skin — Gangrene, ulcers, and sloughs 
— Scars, sweating, dryness, edema, hardness — Anesthesia and hemianes- 
thesia — Paresthesia, hyperesthesia, itching. 

Much information can be obtained by careful examination of the 
skin in many cases of disease. The examiner should make a note 
of the color of the integument, of its general nutrition, of its pliabil- 
ity, and of its sensibility. Naturally the eye at once takes in any 
eruption or scars which may mar its naturally smooth surface, and, 
as eruptions and scars are often the manifestations of more or less 
active systemic disorders, an insight into the presence of internal 
disease may be obtained from them. 



COLOR OF THE SKIN. 

The color of the skin in health in the white race depends upon 
the presence of pigment in the cells of the mucous layer of the 
dermis, and in the corium, in those parts of the body where pig- 
mentation is marked, or to the condition of the subcutaneous circu- 
lation or of the blood in the subcutaneous vessels. Thus we often 
find the skin of the perineum, scrotum, axillae, and of the lower 
abdomen much darker than elsewhere in persons in perfect health. 
Similarly we see a marked reddish or yellowish-brown hue in those 
parts of the skin which have been exposed to sun and weather, as a 
result of a deposition of pigment and an increased capillary cir- 
culation. With these normal alterations in color, however, we have 
little to do, for it is the abnormal colorations which interest us from 
a diagnostic standpoint. 

The most common of these changes in color due to pigment is 
jaundice; the next the chloasma of pregnancy or uterine disease, a 
condition usually limited to the face. Abdominal growths due to 
tuberculosis, cancer or lymphoma, and tuberculosis of the peri- 
toneum also cause pigmentation of the skin, and in melanotic 
cancer there is often very dark discoloration. Again, it is not un- 
common for persons who have hepatic torpor with constipation to 
develop what are called liver spots, and the skin has rather a dirty 



132 THE SKIN 

hue. Under the name of vagabond's " pigmentation" we sometimes 
see discoloration induced by the irritation of the skin produced by 
lice and exposure to dirt and weather. Finally, we see the yellowish- 
brown hue of the skin due to tinea versicolor, the bronzing of 
the skin in Addison's disease, and the slate-blue hue of argyria 
or chronic silver poisoning. (See farther on in this chapter.) 

The changes in color depending upon disturbance of the subcu- 
taneous circulation, or on alterations in the blood, are either local 
or general. In extreme nervousness flushing or blushing, due to a 
local vascular relaxation with increased blood supply, may redden 
the face and neck, and in hectic fever a hyperemia of the skin over 
the malar bones may give rise to an increase in color, which may 
be dusky red, due to imperfect oxidation of the blood. Consider- 
able cyanosis or duskiness of the face and hands in a case of tuber- 
culosis of the lungs is a very grave symptom. Again, we see in 
pneumonia a peculiar dusky red flushing of one cheek or of the 
entire face, and in erysipelas the zone of hyperemic redness is char- 
acterized by its brawniness and its sharp line of demarcation with 
a raised edge. In the alterations in color due to changes in the 
quality of the blood we have, as causes, anemia due to lack of 
corpuscles or of hemoglobin, arising from the various etiological 
factors producing such states. 

Jaundice. — Taking up the color changes due to pigment, we find 
that in jaundice the deposition of the biliary coloring matter varies 
in degree from a slight tinge, or almost imperceptible yellowing, to 
a dark citron or olive-green hue. 

In examining the skin for jaundice care should be taken not to 
do so by gas- or candle-light, for the yellow flame masks the biliary 
color. If the tinge is very slight, it may be made more marked by 
stretching the skin on the palm of the hand or by pressing upon the 
skin a glass slide so that the yellow hue shows through it. 

Having discovered that yellow coloring matter has been deposited 
in the rete mucosum, it remains for the physician to decide what the 
cause of the jaundice may be. In the first place, it must be remem- 
bered that jaundice may be hepatogenous — that is, arise from dis- 
order in the liver and bile ducts, or very rarely be hepatogenous, 
from disorders of the blood with the setting free of blood pigment. 
The hepatogenous jaundice is by far the more common of the two 
conditions, and the most common cause of this form of jaundice is 
catarrhal inflammation of the common bile duct, which in turn 
generally occurs in association with gastroduodenal catarrh. 

Hepatogenous Jaundice. — As a result of a catarrhal process the 
bile duct becomes blocked by the swollen mucous membrane and 
the mucus which is secreted; the biliary coloring matter is ab- 
sorbed into the hepatic circulation and general circulation, and 
is by this means distributed over the body. Another cause of 



COLOR OF THE SKIN 133 

hepatogenous jaundice is the obstruction offered to the flow cf 
bile by the presence of a gall-stone or gall-stones in the duct; and a 
third cause of obstructive jaundice, so called, is pressure on the 
ducts by growths or inflammatory products in the immediately 
adjacent tissues, or of adherent inflammation in the ducts them- 
selves, or rarely by the presence of a roundworm in the common 
duct. Very rarely the jaundice may arise from the pressure on 
the common duct produced by floating kindey. 

Jaundice very rarely arises from pressure on the ducts by an 
aneurysm of the abdominal aorta, or from aneurysm involving the 
hepatic artery. Three such cases are recorded by Frerichs. Jaun- 
dice has also been seen in aneurysm of the superior mesenteric 
artery as the result of pressure, and in cases in which there has 
been, or is, perihepatitis, with displacement of the liver in such a 
way that the adhesions cause twisting or dragging on the ducts. 

Catarrhal jaundice of the acute type is generally produced by 
indiscretions in diet associated with exposure. The patient, after 
more or less marked symptoms of gastric and intestinal disturbance 
and indigestion, feels wretchedly. There is a premonitory mental 
heaviness, with languor and malaise, and within forty-eight hours 
or less the yellowing of the conjunctiva and skin appears. The 
temperature is generally subnormal to a slight degree, but it may 
be febrile. The tongue is heavily coated and often somewhat dry. 
There are marked loss of appetite, great distress, headache, and 
depression of spirits. Examination of the hypochondrium may 
reveal some local tenderness and slight hepatic enlargement, while 
the abdomen will be in some instances markedly tympanitic as a 
result of intestinal fermentative processes in the absence of anti- 
septic bile. The bowels are constipated, often refusing to move 
except with powerful purgatives. There is little pain, except 
headache. This condition lasts for a few days or a week, when the 
yellow color of the skin and conjunctiva usually begins to fade 
and the normal hue is reached in the course of a week or more. 

Other noteworthy symptoms of hepatogenous jaundice are 
intense itching of the skin; a very slow pulse when the patient is at 
rest, due to stimulation of the vagus by the bile in the blood; and 
staining of the sweat due to the bile pigment may also be present. 

The urine in all cases of hepatogenous jaundice is heavily bile- 
stained (see Urine), and the stools are generally clay-colored, owing 
to absence of bile in the feces. 

The presence of persistent jaundice should raise the suspicion that 
it is due to more serious disorder than simple catarrhal inflammation 
such as a growth or stone. 

The jaundice from obstruction by stone may be due to blocking 
of the hepatic duct, whereby there is a stagnation of the flow with 
reabsorption of the bile, or to stoppage of the flow by the presence 



134 THE skin 

of a stone in the common duct just as it enters the bowel. A differ- 
ential diagnosis as to whether the stone is in one or the other of 
these places is usually impossible, but obstruction in the hepatic 
duct is rare. 

The jaundice of gall-stone obstruction may be sudden or gradual 
in onset. If sudden, it is often, but not always, preceded by a 
violent attack of pain in the hypochondrium, or, in other words, 
hepatic colic, in which the agony is excruciating and is accompanied 
by nausea and vomiting. The area of the pain is, however, dis- 
tinctly hepatic, and it does not radiate down the inside of the thigh 
and into the testicle or penis as does that due to renal calculus. In 
place of the subnormal temperature so often seen in catarrhal jaun- 
dice, we find in obstructive jaundice, due to stone, that the tempera- 
ture is often considerably raised, and this is particularly' apt to be 
the case in those instances in which the onset is gradual and the 
jaundice persistent, being due to septic absorption produced by 
the impacted stone, which may be scratching or ulcerating the 
lining membrane of the duct. The history of repeated attacks of 
gall-stone colic, the presence of gall-stones now and then in the 
stools, the discovery of gall-stone crepitus on deep palpation, the 
age of the patient, who is generally in or past middle life, and 
the fact that the patient is often a stout woman who has borne 
several children, all point to gall-stones as a cause of the jaundice, 
but it is a point worth remembering that in many cases there is 
nothing in the history of the patient in the way of pain in the 
gall-bladder and all the discomfort may be referred to the 
stomach. Should the jaundice be due to gall-stones, producing 
irritation or ulceration, so that septic absorption or " Charcot's 
fever" develops, the pulse may become more rapid and running, 
from the general feebleness which rapidly asserts itself. Rigors 
of extreme severity, followed by sweatings and marked febrile 
movement, develop in such cases, the chills occurring daily or 
periodically in a manner closely resembling those of intermittent 
fever. 

As a rule, there is great loss of flesh in all forms of jaundice. 

The jaundice of malignant disease pressing upon the gall ducts is 
usually not intense, and is characterized by the physical signs of a 
tumor, by the marked wasting of the patient, and, as a rule, by the 
very gradual onset of the pigmentation of the skin. Generally the 
lesion in such cases is carcinoma of the head of the pancreas. In 
jaundice resulting from cancer of the liver the growth must be so 
situated as to compress the ducts, consequently jaundice occurs in 
only about one- third of such cases. 

In connection with this possibility the law of Courvoisier is to be 
borne in mind. This law has been well expressed by Mayo Robson 
in the following words: "Jaundice with distended gall-bladder is 



COLOR OF THE SKIN 135 

presumptive evidence in favor of malignant disease, but jaundice 
without distended gall-bladder favors the diagnosis of cholelithi- 
asis." While this rule is a good guide, it must not be forgotten, 
as pointed out by Kehr, that gall-stones produce malignant disease. 
Thus Courvoisier found gall-stones in 87.5 per cent, of malignant 
cases, Delano Ames in 95.4 per cent, of gall-bladder cancer, and 
Schroeder has reached similar conclusions. 

Jaundice is also seen in hepatic hypertrophic cirrhosis to a slight 
extent in a small proportion of cases, and it is to be remembered 
that in those cases of this disease in which delirium and muscular 
twitching occur the symptoms may resemble acute yellow atrophy 
of the liver, but all forms of jaundice often produce headache and 
may cause delirium. In acute yellow atrophy of the liver (see below) 
the liver is greatly reduced in size, whereas in hypertrophy it is 
greatly increased in size ; and in atrophy the temperature is subnor- 
mal, whereas in the jaundice due to hypertrophic cirrhosis it is apt 
to be above normal. Jaundice also may be a manifestation of acute 
poisoning by phosphorus, which condition is generally accompanied 
by hepatic swelling and tenderness and with coffee-ground vomiting. 

A moderate degree of jaundice is sometimes seen in cases' of 
chronic valvular cardiac disease in which compensation is gradu- 
ally failing. Rarely this hue becomes deeper as the heart failure 
increases. This jaundice is due to engorgement of the liver, which 
in time results in catarrh of the bile ducts, with consequent 
obstruction to the flow of bile. 

In amyloid disease of the liver Bartholow states that jaundice 
occurs in about one-tenth of the cases as a result of enlargement of 
the lymphatics in the hilus with pressure on the hepatic duct. 
Similarly jaundice may result from the presence of echinococci, but 
this is not a common symptom of the growth of these parasites, and 
the disease is almost unknown in the United States and England 
except in travellers. 

Jaundice sometimes complicates glycosuria. Under these circum- 
stances it may be regarded as a coincidence or a valuable diagnostic 
aid, for, as we have already stated, tumors of the pancreas by press- 
ing on the common duct may cause jaundice, and, as is now well 
known, widespread disease of the pancreas may cause glycosuria. 
Jaundice in a case of diabetes should, therefore, direct attention to 
the pancreas. 

In this connection it is well to remember that Hanot, under the 
name of diabete bronze, has described a pigmentation of the skin 
which contains iron (that of Addison's disease and melanemia does 
not), and which is associated with glycosuria, hypertrophic cirrhosis 
of the liver, and enlargement of the spleen. The coloration occurs 
most markedly upon the face, limbs, and genital organs; the glyco- 
suria is abundant and slight ascites may be present, the lower limbs 



136 THE SKIN 

may be edematous, the loss of weight and strength is rapid, and 
death soon ensues from pneumonia or coma. Hanot and Marie 
both regard it as a disease distinct from ordinary diabetes mellitus. 
True diabete bronze is exceedingly rare. 

A very rare cause of jaundice is acute yellow atrophy of the liver, 
a disease which is seen somewhat more frequently in women than 
in men, and particularly in association with pregnancy. The age 
of occurrence is usually between the twentieth and thirtieth years. 
The symptoms begin with gastro-intestinal disorder, followed by 
headache, delirium, muscular twitching, and perhaps convulsions. 
Simultaneously with the onset of the headache the jaundice appears, 
the patient becomes typhoidal and dies from exhaustion. The 
stools during the attack are clay-colored, and the urine contains 
leucin in disks and tyrosin in needle-like crystals. 

Hematogenous Jaundice, which is very rarely met with, is due, as 
its name implies, to breaking down of the blood to so great an 
extent that the liver cannot deal with the waste material with 
sufficient rapidity, and as a result altered hemoglobin is desposited 
in the tissues. Any poison which produces excessive hemolysis, 
such as picric acid and the coal-tar products, chlorate of potassium, 
glycerin, and poisonous mushrooms, may cause this condition to 
develop, and in extreme malarial disease (remittent and pernicious 
malarial fever), dengue, relapsing fever, pernicious anemia, pneu- 
monia, and in other infectious maladies, jaundice may be produced 
in this manner. It develops sometimes in cases of marked sepsis. 

Jaundice is present in all fatal cases of yellow fever and often in 
cases which ultimately recover. It also is a constant symptom in 
that very rare malady, Weil's disease, which is probably in reality 
a septic icterus, but it is very seldom seen in suppurative hepatitis. 

Jaundice sometimes occurs after severe hemorrhage of a pro- 
longed character and in prolonged exhausting fevers, and is then due 
not to any local hepatic trouble, but to blood changes, with the 
production of urobilin in excessive amounts. The urine fails to 
carry off all the urobilin which is produced from hematoidin or 
bilirubin. This condition is called " urobilin icterus." 

In nearly all cases of hematogenous jaundice the discoloration of 
the skin is very slight, and the important fact is to be remembered 
that the stools are not light or clay-colored as in hepatic jaundice, 
but contain a normal or excessive amount of pigment. Again, the 
systemic symptoms of catarrhal or obstructive hepatic jaundice are 
practically absent in the hematogenous variety, and the jaundice is 
simply a minor symptom associated with more grave manifesta- 
tions which characterize the individual infectious process. If the 
toxemia is very marked, convulsions, coma, or active delirium 
may come on, but it is probable that these symptoms are due 
more to the poison of the disease than to the broken-down blood. 



COLOR OF THE SKIN 137 

Vierordt states that a very small amount of biliary coloring 
matter is often found in the urine of patients suffering from pyemic 
jaundice, and regards this as an important sign that the discolor- 
ation of the skin is due in a given case to blood changes and not to 
biliary obstruction, whereas an excessive amount of biliary matter 
in the urine indicates hepatic trouble. 

When hematogenous jaundice complicates croupous pneumonia, 
it usually indicates a fatal ending, but when it arises from catarrh 
of the gall ducts during an attack of pneumonia the condition is 
by no means so grave. 

Jaundice sometimes comes on in the course of acute ulcerative 
endocarditis, and has been mistaken for that of acute yellow atrophy 
of the liver, and it often appears as a symptom of pernicious malarial 
fever, with vomiting, diarrhea, and grave nervous symptoms. 

Rarely jaundice follows severe fright or extreme anger, and 
J. M. Da Costa stated that it sometimes ensues after concussion 
of the brain. 

There remains to be considered the jaundice seen in the newborn, 
usually within the first or second day of life (icterus neonatorum). 
Some believe it to be due to a decrease in the blood pressure in 
the portal vessels subsequent to the arrest of the placental circula- 
tion, with consequent absorption of bile into the blood, owing to 
the comparatively high tension of this fluid in the bile capillaries. 
Others think this jaundice is due to breaking down of the blood 
corpuscles shortly after birth as the result of some mild infection. 
Probably both causes act in many cases. If the cause be altered 
blood pressure the prognosis is favorable, and recovery takes place 
in about ten days or two weeks; but if the cause be an infection, 
the condition often proves rapidly fatal. Should this jaundice of 
the newborn be very marked the patient may be suffering from 
congenital stenosis, or absence of, the common or hepatic duct 
(which cause is rare); from septicemia, through infection by way 
of the umbilicus; from phlebitis of the umbilical vein, or from a 
hepatitis due to hereditary syphilis. In any of these latter causes 
death will probably occur, whereas in the mild form of icterus 
neonatorum the prognosis is very favorable, even though the dis- 
coloration lasts for weeks. The mild form of icterus neonatorum, 
if due to blood changes, is rarely accompanied by great discolor- 
ation of the urine, and the feces are usually no lighter in color than 
normal; but if hepatic disease be present, the urine is bile-stained 
and the feces are light in hue. 

Other Changes in the Color of the Skin. — When the skin of the 
entire body, the face being particularly affected, is of a livid or 
bluish-slate color, resembling somewhat the appearance of a person 
exposed to rays of light passing through blue glass, the condition 
is that of argyria or chronic silver poisoning. This discoloration 



138 THE SKIN 

is so characteristic as to admit of no difficulty in diagnosis, since 
the absence of any circulatory or respiratory embarrassment 
excludes the possibility of its being due to cyanosis. Owing to 
the small amount of silver now given internally by physicians, 
chronic argyria is very rare. The discoloration is due to a deposit 
of oxide of silver in the rete Malpighii. 

Discoloration of the skin of the entire body of a sallow, lemon- 
yellow tint, sometimes called a "muddy yellow" hue, is seen in 
persons who are sufferers from prolonged malarial poisoning, and in 
some cases the subjects of prolonged suppurative processes not 
tuberculous in character. A greasy, yellowish skin does, however, 
occur as an accompaniment of some cases of pulmonary phthisis, 
and these cases have, as a rule, a gloomy prognosis. Often chronic 
hepatic disease, such as cirrhosis, produces this sallow appearance, 
but the skin is usually wrinkled and dry. 

A very rare but interesting condition of dark discoloration of 
the skin is met with in cases of ochronosis. Associated with this 
discoloration there is a similar darkening of the conjunctiva, which 
is particularly well marked at the angles of the palpebral fissure, 
and alkaptonuria, that curious state in which the urine reduces 
copper in Fehling's test, although sugar is absent. Autopsy reveals 
an intense darkening of the articular cartilages. 

Other changes in the color of the skin, which cannot be said to 
be due to deposition of pigment, although they seem to be caused 
by this, are seen most markedly in the peculiar yellowish, cheesy 
pallor of carcinoma, the greenish-yellow tinge of true chlorosis, the 
curious cadaveric hue of advanced pyemia, and the yellow skin 
with a greasy feeling in some cases of paretic dementia. 

Local pigmentation of the skin results from many causes, both 
local and systemic, direct and indirect. When brownish-yellow 
spots or streaks appear on the face, so that chloasma is developed, 
we should look for uterine or hepatic disturbance, or pregnancy; 
they are practically large freckles of a more or less distinct brown 
hue. Sometimes on the skin of the trunk, small yellowish-brown 
or chamois-skin colored spots appear accompanied by no other 
symptoms except perhaps slight itching. This is due to phthiriasis 
versicolor or chromophytosis, due to the growth of the parasite 
microsporon furfur. The diagnosis can be settled by painting the 
infected area with Lugol's iodine solution, when the spot becomes 
a dark-brown or mahogany color. This is called "Allen's test." 
In other instances chloasmic spots or localized discoloration of the 
skin results from injury to the skin, as pressure by clothes, charing, 
or after constant severe scratching in the course of eczema or 
pediculosis or scabies. If the pigment is found in the nuchal and 
sacral regions, it is probably from the scratching caused by pediculi; 
if on the body in irregular distribution, it may have been caused by 



COLOR OF THE SKIN 1 39 

prurigo. Again, the presence of a brown pigmentation of the skin 
in a clearly outlined patch may indicate the earlier use of a fly 
blister, a mustard plaster, or other counter-irritants, and a brown 
discoloration of the skin, which might possibly be confused with 
that of Addison's disease, is produced by the free use externally of 
oil of cade. Sometimes these spots are produced by the prolonged 
use of arsenic, and the writer has reported a case in which the 
coalescence of the spots produced a curious grayish-brown hue 
of the entire body, so that the man looked somewhat like a mulatto. 

Sometimes brown pigmentation of the skin of the neck and face 
appears as a symptom in exophthalmic goitre, and this disease may 
also produce similar lesions on the chest and wrists. 

Very closely resembling these spots is the bronzing of the skin 
in patches which is seen in persons suffering from Addison's dis- 
ease; but although bronzing of the skin is a somewhat constant 
symptom of Addison's disease, its presence is neither a positive nor 
negative sign in diagnosis, for bronzing is sometimes seen in cases 
in which the suprarenal capsules are normal. In some instances 
the bronze color deepens into a dark gray or even a black hue, and 
although the discoloration is generally in patches, it may extend 
over the entire surface of the skin, even to the edges of the finger 
nails. The nails, however, escape, as does also the mucous mem- 
brane of the lips, although the lining of the mouth itself may be 
dotted with pigmentation. The color is due to pigmentation of the 
rete Malpighii, and pressure has no effect on it. The symptoms of 
Addison's disease to be found associated with these skin changes are 
" anemia, general languor or debility, remarkable feebleness of the 
heart's action, and irritability of the stomach." 

White patches, or leukoderma, are also sometimes seen in cases of 
true goitre, and brown ones in tuberculosis. 

In carcinoma of one of the internal organs, or of the breast of 
an advanced stage, the appearance of the skin is drawn and unusu- 
ally smooth, often shiny or greasy looking, somewhat gummy and 
leathery to the touch, particularly where the integument is naturally 
dense. Although it is difficult to describe, this skin is almost path- 
ognomonic of carcinoma, although it may also be present to some 
extent in far-advanced cases of pernicious anemia or sarcoma. 

Pallor of the skin is due to absence of the normal pigment and 
to deficient blood, as in fainting. As a type of the pallor due to 
lack of pigment in the skin we see vitiligo, while the pallor due to 
pernicious anemia or chlorosis and hemoglobin is owing to lack of 
red corpuscles. In chlorosis the entire surface of the body is 
exceedingly pale, and the skin of the face, particularly about the 
mouth and nose and eyes, is somewhat greenish in hue. The skin 
of the cheeks may, however, be flushed and the lips abnormally 
red in hue. A very important diagnostic point to be remembered 



140 THE SKIN 

is that red cheeks often cause the physician to overlook well- 
advanced anemia in young women. The skin is apt also to be 
very white, and even chalky in appearance, in chronic contracted 
kidney and chronic parenchymatous nephritis. 

In those cases in which the skin is pale from alteration of the 
subcutaneous circulation there is usually incompetence of the heart 
or vasomotor disturbance, but the most marked form of general 
pallor is that due to myxedema or cretinisn. (See below.) 

Cyanosis, or blueness of the skin, depends upon the circulation in 
the cutaneous vessels of imperfectly oxidized blood. The small 
veins are often seen to be swollen, particularly those of the face and 
the hands and feet. 

The most marked form of cyanosis with which we meet is the 
cyanosis of the newborn child, suffering from a patulous foramen 
ovale, and in this condition the color may vary from a slate hue 
to an almost black hue. The lobes of the ears, the tongue, the 
scrotum, and the toes show the color most deeply. It is important 
to remember that this form of cyanosis is greatly decreased, as a 
rule, by placing the child on its right side. Anything which pro- 
duces excitement increases the cyanosis greatly, whereas cyanosis 
due to other causes is not subject to such great variations. In the 
cyanosis of the newly born, males are far more frequently affected 
than females, in the proportion of about 2 to 1 or 3 to 1, and it is a 
noteworthy fact that even when the cyanosis is due to a malforma- 
tion of the heart it may not be present from the time of birth, but 
may develop several days afterward. J. Lewis Smith recorded 41 
cases in which the cyanosis due to congenital heart lesion came on at 
periods ranging from two weeks to forty years after birth. 

In cyanosis of the newborn the chances are about 10 to 1 that 
the lesion is absence of a properly developed interauricular or 
interventricular wall. About 35 per cent, of the cases of cyanosis 
due to congenital defects die in the first year. 

In the adult or child cyanosis may be produced by serious cardiac 
disease, by pulmonary disease, such as pneumonia, pulmonary con- 
gestion, and bronchiectasis with emphysema and associated cardiac 
dilatation. It also occurs in laryngeal obstruction arising from 
external pressure or intralaryngeal difficulty, and in cases of asthma 
of a severe form. (See chapter on the Thorax and its Viscera.) 

In other instances a grayish-blue or cyanotic appearance may 
arise from the ingestion of drugs which reduce the hemoglobin of 
the blood, such as antipyrine or acetanilid, and in such instances 
the discoloration is first seen about the base of the thumb nail or 
in the skin of the face, particularly if the patient be examined from 
a little distance. 

In some cases of paretic dementia the skin of the forehead is dull 
and dusky-looking. 



ERUPTIONS ON THE SKIN 141 

A condition of the skin characterized by yellow, more or less 
elevated patches is xanthoma, which Murchison states often com- 
plicates hepatic disease, but in the writer's experience it is more 
commonly met with in gouty women past the menopause. Its 
favorite distribution is about the lower eyelids, but it may appear 
elsewhere. Lesions similar to xanthoma sometimes appear in the 
course of diabetes (Hutchinson, Besnier), and under these circum- 
stances generally develop suddenly, and spontaneously disappear 
after some weeks or months. 

The condition of the skin, so far as its nutrition is concerned, is 
of great importance in diagnosis. In profound failure of the vital 
forces continuing over a great length of time it becomes abnormally 
dry and scaly, the hair becomes straggling and lustreless, and fre- 
quently falls. In young persons suffering from grave disease of the 
lungs or heart of a chronic type there is often not only an undue 
dryness of the cuticle, but an abnormal growth of downy hair all 
over the body and limbs, and more particularly down the spine and 
over the breast bone. 



ERUPTIONS ON THE SKIN. 

The influence of age upon the development of skin lesions is 
very great, and Stephen Mackenzie has summed up the relation- 
ship of skin diseases to age in the following amusing manner: 
"The seven stages of man could well be illustrated by disease of the 
skin, though we lack a Shakespeare to do justice to the theme. In 
the 'mewling and puking' infant we meet with sclerema and edema 
neonatorum, the 'red gum' or strophulus of the older writers, inter- 
trigo, eczema, urticaria papillosa (lichen urticatus), urticaria pig- 
mentosa, xeroderma pigmentosum, and impetigo; the 'school-boy,' 
with his chilblains and ring-worms, alopecia areata, pityriasis rosea, 
ecthyma, and 'foot-ball disease;' and then the 'lover,' with his acne 
and sycosis, and, as a result of irregular sexual excursions, his 
syphilides; 'and then the justice, in fair round belly,' with acne 
rosacea, diabetic boils, and pruritus ani; the sixth stage shifts into 
the 'lean and slippered pantaloon,' with rodent ulcer and 'gouty' 
eczema; last scene of all, sans teeth, sans eyes, sans taste, sane 
everything' — except an incessant and intolerable itching of the 
skin which we call senile prurigo." 

There are three conditions of the skin or subcutaneous tissues 
sometimes found in patients suffering from rheumatism. One is 
the presence of erythema in one of its many forms, another is the 
appearance of purpura, or, as it has been called, peliosis rheumatica. 
The third lesion is subcutaneous fibroid nodules which vary in size 
from a small shot to a large pea. They occur chiefly about the 



142 THE. SKIN 

fingers and hands, but also on the back, elbows, and knees. Usually 
they are permanent, but they may be fleeting. 

That the presence of erythema is often associated with lithemic 
or true rheumatic infection is proved beyond all doubt, either 
erythema papulatum, annulaire, marginatum, or nodosum being 
indicative of the systemic state, but it is worthy of note that 
the erythema marginatum is most diagnostic and erythema nodo- 
sum the least diagnostic of rheumatic poisoning. Sometimes this 
eruption may be the only manifestation of the disease other than 
cardiac involvement, and when it is marginate severe cardiac 
lesions are commonly present. The papulate eruption is most 
commonly found on the back of the wrists, the hands, and the 
feet when it occurs as a rheumatic sign, while the nodose variety 
is generally confined to the front aspect of the legs or the extensor 
surfaces of the arms. It is to be remembered that these forms of 
erythema may be distributed anywhere over the body in rheu- 
matism, but that they become especially diagnostic if limited to 
the areas named. (See Erythema or Rose Rash.) 

Purpuric Discolorations of the skin, somewhat resembling minute 
multiple bruises in appearance, are due to a number of causes and 
possess a varied significance. In the first place, they are due to the 
condition known as purpura hemorrhagica, which may be divided 
into the acute and subacute forms and that which is secondary 
to severe infections and certain poisonings. The acute fulminant 
form of purpura, which is probably in all cases a manifestation of 
an infection by a pathogenic organism, runs a rapid course and 
reaches a fatal result in most cases in a short time. It is a com- 
paratively rare disease and usually attacks young adults, chiefly 
males, up to twenty-eight years of age. It is sometimes seen in 
young girls and more rarely in young pregnant women. The chief 
symptoms consist in hemorrhages from the mucous membranes, 
purpuric spots, high fever, and a general class of symptoms 
resembling those of sepsis, as chills, pyrexia, and exhaustion. In 
other instances active hemorrhages take place into the viscera, 
and if into the meninges of the brain cause cerebral symptoms at 
once. The liver and spleen are nearly always enlarged. 

The subacute type of purpura, while severe, runs a far more favor- 
able course as to its manifestations and results. It usually attacks 
children or young adult males from twenty to thirty years of age. 
The patient, after a feeling of wretchedness, and perhaps a chill, 
followed by the purpuric eruption, is attacked by swelling of the 
joints and perhaps hemorrhages from the kidneys, bowels, and 
mucous membranes. If the hemorrhage is from the gums, the teeth 
are not loosened, as in scurvy. Prostration may be great and the 
patient may appear as if suffering from typhoid fever. The prog- 
nosis is good for ultimate recovery. It is sometimes called peliosis 



ERUPTIONS ON THE SKIN 143 

rheumatica, or Schonlein's disease. This subacute form, however, 
sometimes occurs in a more severe manner, as "Henoch's disease," 
in children between nine and twelve years, and is much more 
common in males than females (5 to i). In this form we have 
as additional symptoms marked pain and tenderness in the belly, 
and bloody stools, with tenesmus and active vomiting. The illness 
may last a long time, but recovery often occurs, about 25 per cent, 
dying. 

The joint symptoms of the mild forms of purpura may be slight 
or absent. Often, too, the purpura is accompanied or replaced by 
erythema. 

The question as to whether purpuric eruptions are ever truly 
indicative of rheumatism has been much discussed. When purpura 
develops in the course of true articular rheumatism it is often an 
indication of an associated infection. In many cases, however, the 
arthritic inflammation is not a true rheumatism but in reality a 
septic arthritis which is due to the same cause as the purpura. In 
either case the eruption appears as a rule in the neighborhood of 
the involved joints, nearly always on the lower limbs, often breaking 
out before any evidence of articular trouble exists. In other in- 
stances the development of the purpura is simultaneous with the 
disappearance of joint trouble. The eruption usually fades in a 
few days, but frequent relapses or new crops of it often occur. 

Purpuric eruptions may be produced by quinine in persons who 
have an idiosyncrasy to this drug, and by iodide of potassium, 
chloral, and salicylic acid. They may also accompany any severe 
infectious disease and follow the entrance into the body of any 
poison which profoundly alters the blood, such as the poison of 
snake bite. They also result from severe jaundice, from profound 
anemia, from congenital syphilis with vascular changes, in ulcer- 
ative endocarditis (a form of sepsis), and in cases of multiple 
sarcomata. Rarely purpura has followed fright and severe grief. 

Petechias sometimes appear in the skin covering a part which 
has been affected by a severe pain in a crisis of locomotor ataxia. 

A very extraordinary manifestation of spontaneous subcutaneous 
hemorrhage is seen in what is known as hematoma auris, a condi- 
tion in which a free extravasation of blood takes place into and 
beneath the skin of the ear. The color of the swollen ear is quite 
red, if the hemorrhage has been recent, or dark blue if it is an old 
occurrence. The left ear is more commonly affected than the right, 
and it is seen more commonly in paretic males than in females. 

The development of polymorphic skin lesions, consisting of hyper- 
emia, edema, and hemorrhage, with arthritis occasionally and vis- 
ceral disturbances, consisting in attacks of vomiting or diarrhea, 
endocarditis, pericarditis, acute nephritis, and hemorrhages from the 
mucous membranes, indicates the presence of a condition called 



144 THE SKIN 

erythema exudativum multiforme. The attacks are apt to be recur- 
rent. Sometimes the skin manifestations are absent. 

Redness of the skin is seen in acute inflammations of the skin 
or the subcutaneous tissues as in erysipelas, and as the result of 
hot applications, the redness being marked in proportion to the 
degree of heat and the length of time it is applied. Often the 
prolonged use of high heat will produce a peculiar mottling of the 
skin like that of an old bruise. 

Aside from the redness of the cheeks and forehead from blushing, 
we should remember the general flushing seen so commonly in 
persons suffering from phthisis, particularly when they are excited, 
which differs from the more dusky redness seen over the malar 
bones in hectic fever and the morbid flushing of the chloral and 
morphine habitue. 

Another interesting diagnostic sign in the skin is what is known 
as the u tache cerebrate" a condition of vasomotor disorder in which 
when the finger is gently drawn over the skin of the forehead a red 
patch speedily develops. It is seen in meningeal irritation, brain 
abscess, epilepsy, in some cases of exophthalmic goitre, and in 
paretic dementia. Sometimes it is called u tache meningeale" 

Erysipelas. — A dusky-red rash rapidly spreading over the neigh- 
boring skin, above the level of which the affected area is raised, and 
which is separated from the sound skin by a sharp line of demar- 
cation which can be both seen and felt, is characteristic of erysipelas. 
The skin soon becomes brawny to the sight and touch, and the lines 
of demarcation feel markedly indurated. Most commonly the dis- 
ease appears on the face, starting from the inner can thus of the 
eye, the nostril, or the corner of the mouth. Rarely erysipelas 
affects the skin of the trunk. The fever may be quite marked, even 
in mild cases, and usually falls by crisis on the sixth day. In 
severe cases with fatal tendencies there may develop in place of 
crisis a typhoid state with low fever and delirium. If the disease 
be severe, blebs and bullae form, edema of the skin becomes very 
profound, and finally suppuration may occur, forming what is 
known as phlegmonous erysipelas. (See also Glanders.) Ery- 
sipelatous inflammation of the skin without systemic disturbance 
may follow the application of arnica. 

A condition also closely resembling erysipelas in its raised surface 
is urticaria, which, however, differs so materially in other respects 
that a diagnosis is readily made. Aside from the absence of 
systemic disturbance in urticaria the swelling of the skin is net 
red, but pale and pearly in hue, although it may be surrounded 
by an erythematous blush; the onset is extraordinarily sudden, so 
that a skin seemingly normal at one moment, after a slight bruising 
by the finger or rubbing by the clothes, develops the complete 
eruption in a moment. 



ERUPTIONS ON THE SKIN 145 

Anthrax. — The development of a painless macule on the skin of the 
hand or foot, followed by an acutely inflamed papule which itches 
and is soon changed into a relaxed vesicle containing bloody serum, 
in which there is a hard nucleus which rests upon an indurated base, 
is the initial manifestation of anthrax maligna or malignant pustule. 
The lymphatics soon become swollen, and metastatic abscesses 
speedily form elsewhere, as in the axillary glands. The systemic 
symptoms are severe, sometimes being manifested in high fever, in 
other cases by a typhoid state. Death is very commonly the sequel 
(65 per cent.), even if prompt surgical interference takes place. 
There is generally a history of exposure to infected animals or 
their hides. Malignant pustule is to be separated from carbuncle 
by its fulminating character and peculiar appearance. 

Glanders. — When an erysipelatoid rash with swelling of the skin 
and the development of papules, vesicles, pustules, and bullae 
appears in association with induration of the skin, with sloughing 
eventually taking place, the disease may possibly not be erysipelas 
of a phlegmonous form, but glanders or equina. Numerous in- 
flammatory foci appear in the skin in glanders which end in local 
abscesses and hemorrhagic nodules, and profound systemic infec- 
tion is always present. The presence of a sanious discharge from 
the nose aids in confirming the diagnosis. Death usually comes in a 
few days in this acute form. Should the course of glanders be 
chronic, pustules somewhat like those of smallpox, except that they 
are not umbilicated, lie on an indurated base, and in them is formed 
a viscid or sanious pus of offensive odor. This disease is rare. 
Both forms arise from infection from a horse suffering from the 
malady. Glanders may be confused with variola or the pustular 
and ulcerative gummatous stages of syphilis. 

Urticaria may occur as a manifestation of rheumatism, but it has 
no diagnostic value. Sometimes it ensues upon the use of salicylic 
acid or turpentine, and quite commonly follows the ingestion of 
iodide of potassium. The wheals produced by the latter drug differ 
from those of ordinary urticaria in being unduly red. In some 
persons it follows the eating of strawberries or other acid fruits 
and the ingestion of shell-fish. 

Angioneurotic Edema. — Very closely allied in appearance with 
urticaria of a severe type is angioneurotic edema. In this condition 
there appear upon the skin numerous patches or plaques of cir- 
cumscribed puffy swellings, which have a red appearance and vary 
from the size of a nickel to a silver dollar or larger. There is an 
absence if itching, an important difference from true urticaria, 
but the part affected may be tense or hot to the patient. These 
attacks are generally recurrent, and take place in neurotic persons. 
They may cause loss of sight through swelling of the eyelids, and, 
where the mucous membranes of the nasopharynx and larynx are 
10 



146 THE SKIN 

involved, serious interference with breathing. The swelling of 
angioneurotic edema does not pit, and it is to be separated from 
the blue edema and white edema of hysteria. True angioneurotic 
edema is rare in hysteria, but if localized swellings do result from 
this condition the physician will generally find marked hysterical 
signs manifested, such as disorders of sensation or tenderness over 
the ovaries. (See Raynaud's Disease.) 

Erythema or Rose Rash, sometimes called roseola, is a redness of 
the skin, and occurs in many pathological conditions. It may be 
localized or diffused. In a number of diseases it aids very greatly in 
reaching a diagnosis, but the physician should always be cautious 
in depending much upon it, since it may mislead, owing to the fact 
that it often appears when devoid of diagnostic importance insofar 
as the eruptive fevers are concerned. (See below.) 

An erythema or roseola sometimes appears on the skin of chil- 
dren after vaccination, generally about eight to ten days after the 
operation. It rarely lasts more than two days, and on its disap- 
pearance there is slight desquamation. 

It also appears sometimes in cases of smallpox previous to the 
outbreak of the true eruption. Under the latter circumstances it is 
found most commonly about the groin and inner surface of the 
thighs and on the hypogastrium, loins, clavicles, and the extensor 
surfaces. 

The Rash of the Acute Infectious Diseases. — The development 
of a diffuse, punctated rose rash on the skin of a person who is suffer- 
ing from malaise, fever, nervous disturbance, and sore throat should 
direct the physician's attention to the possible presence of two 
infectious diseases, namely, scarlet fever, which is more common 
in childhood, and syphilis, which is more frequent in adults. 

Scarlet Fever. — The rash of scarlet fever is usually of a bright-red 
color, and shows itself at the end of the first or on the second day of 
the disease, first appears on the chest and neck, and then speedily 
involves nearly the whole surface of the body, although the forehead 
often escapes and the skin about the corners of the nose and mouth 
is nearly always very white and free from eruption. On the other 
hand, the soles of the feet and palms of the hands are very markedly 
affected. So intensely reddened is the patient's surface that it may 
have the color of a boiled lobster. In some cases, however, the 
eruption does not extend over the whole surface. This redness de- 
pends upon an acute hyperemia of the skin, which though removed 
by pressure instantly returns when the finger is withdrawn. A 
noteworthy point is its punctate and mottled appearance, for, 
while the entire skin may be red, there are points which are more 
red than the rest of the skin, and also certain areas which are 
particularly so. The skin is often slightly swollen and feels tense 
and hot, and itching is commonly present. The rash usually lasts 



ERUPTIONS ON THE SKIN 147 

from three to seven days, and then fades, desquamation of the cuticle 
setting in in about two or three weeks. Often when the rash can 
scarcely be seen on the skin its full development will be found on the 
pharyngeal wall. In the malignant types of scarlet fever petechias 
and subdermal hemorrhages occur. Sometimes in scarlet fever 
fine miliary vesicles develop chiefly in the neighborhood of the 
axillae or on the abdominal wall or thorax anteriorly. 

Sometimes, too, in those cases of scarlet fever which have severe 
symptoms of ulcerating sore throat, with ear or nose complications, 
there develops, about the third week of the disease, a dark-red 
papular or macular erythema on the extensor aspects cf the large 
joints. It is a grave symptom. 

An erythema resembling scarlet fever, not only in its appearance 
but also by its association with swelling of the lymphatic glands 
and reddening of the mucous membranes of the mouth, sometimes 
develops about the second or third day in cases of dengue or break- 
bone fever. 

In children there are several other conditions than scarlet fever 
which are associated with rose rash, and these are prone to lead 
to grave errors of diagnosis not only because they may be mis- 
taken for scarlet fever but chiefly because a mild attack of scarlet 
fever may be mistaken for them. The most frequent of these is 
erythema roseola, or roseola of acute indigestion, or that following 
the use of a food to which the patient has an idiosyncrasy. It 
is generally, but not always, widely diffused and is often associ- 
ated with acute and severe febrile movement and vomiting, but it 
can be separated from scarlet fever by the facts that there is an 
absence of severe constitutional and nervous symptoms (except in 
neurotic children), there is no sore throat or enlarged cervical glands, 
and the rash does not come out on the clavicles and gradually 
travel down the body. Roseolous eruptions also appear in persons 
with delicate skins after coming in contact with irritant plants 
as rhus, and Dukes asserts that they may develop from handling 
caterpillars. 

The severe cases of scarlatina are easy of diagnosis. It is those 
in which the rash and sore throat are mild that are difficult of deter- 
mination. In these cases the physician must delay his diagnosis 
until the subsequent course of the malady enables him to marshal 
before his mind's eye most of the characteristic manifestations of 
true scarlet fever. 

When roseola develops after a surgical operation or after delivery 
in a puerperal female, it is not a manifestation of scarlet fever, but 
is due to sepsis (" surgical scarlet fever"), although it is, of course. 
possible for scarlet fever to attack such cases at any time. The 
rash is usually found over the abdomen and inner sides of the 
thighs. The absence of sore throat, the presence of a septic 



148 THE SKIN 

process, and the absence of a strawberry tongue all help to exclude 
scarlatina. Sometimes late in an attack of cholera a rash-like 
surgical roseola appears in the same, areas, or in the period of 
reaction comes out on the forearms, backs of the hands, and rarely 
on the back. 

Another condition closely resembling scarlet fever is rarely seen, 
namely, acute exfoliating dermatitis, called, in its mild form, ery- 
thema scarlatiniform, which has a sudden onset with febrile move- 
ment and a rash which rapidly spreads over the entire body and 
lasts four or five days, finally ending in desquamation. So closely 
may this disease resemble scarlet fever that a diagnosis during the 
first attack may be impossible for the first few days, but the con- 
dition of the throat and tongue does not resemble the condition 
seen in scarlatina. Desquamation is often even more complete 
than in scarlatina, and the hair and nails are frequently shed. 
Relapses are very common and give rise to the reported cases of 
repeated attacks of scarlet fever. 

Among other diseases in which rose rash appears we find diph- 
theria, septicemia, cholera, typhoid fever, malarial poisoning, and 
Bright's disease. In diphtheria it may lead the physician to a 
diagnosis of scarlet fever with severe faucial manifestations, and 
only a careful examination of the throat, the rapid subsidence of the 
rash, and the bacteriological examination of the false membrane 
will settle the diagnosis. Sometimes, however, a roseola appears 
late in the course of diphtheria, probably as a result of septic 
absorption. In other instances the injection of antidiphtheritic 
serum or other antitoxins produces this result. The presence of a 
very high temperature, of nervous irritability, and the predomi- 
nance of the throat lesions of scarlet fever ought to decide the 
diagnosis in favor of scarlet fever. 

The physician should also recall the fact that the injection of 
antidiphtheritic serum sometimes causes a roseolous eruption, asso- 
ciated, it may be, with pains in the joints. The general illness 
caused by diphtheria, plus these symptoms, may point to a com- 
plicating scarlet fever or measles. The antitoxin rash is not, as a 
rule, so persistent as that of scarlet fever, lasts a short time, and is 
rarely followed by desquamation, except in fine scales. While it 
may resemble measles in its characteristics, the patient does not 
present the eruption on the pharyngeal mucous membrane nor 
the peculiar coryza of that disease, nor the bronchitis or other 
evidences of respiratory catarrh, nor Koplik's spots. 

The roseola of early syphilis resembles that of scarlet fever in 
that it first appears on the trunk; it is not bright scarlet, but 
rather dusky red. It appears in patches and is not diffuse, and it 
ensues about six weeks or three months after the appearance of the 
initial lesion, occurs in an adult, as a rule, is not associated with 



ERUPTIONS ON THE SKIN 1 49 

high fever, and soon involves the face and forehead. These symp- 
toms aid us in separating it from scarlet fever, although the rash 
often appears in full blast in the palms of the hands and soles of 
the feet; but a roseolous rash in these areas in an adult is always 
suspicious of specific trouble. These patches speedily change from 
rose rash to other more marked lesions in cases of syphilis, and one 
of the first changes that they undergo is to become circinate. They 
fade and reappear, last an indefinite time, fade in the centre, and so 
change into marginate or circinate erythema. 

When the roseola becomes transformed into slightly elevated 
or bean-shaped spots, irregularly scattered, but sometimes forming 
groups which are apt to be circular, and these circles become mar- 
ginated and then scaly on the edges resembling lepra or psoriasis, 
or even go further than this and develop bullae and blebs, and 
when the sores which form are filled with a clear liquid which 
may become sanious or turbid and on drying leave crusts, the 
removal of which reveals deeply excavated sloughs, the area of 
the slough often being as large as a silver dollar, but often irregular 
in outline, syphilitic rupia is probably the lesion. There is, how- 
ever, this important differential point, namely, that in specific 
rupia there is an essential feature, a peripheral ring of induration, 
whereas in the non-specific form this induration is absent. 

If, in addition to these variations, the eruptions are dusky red 
and leave behind them on healing copperish-looking discoloration 
of the skin, and appear on areas, such as the flexor surfaces, where 
ordinary skin eruptions are rarely seen, the diagnosis of syphilis is 
highly probable. If the eruption is chiefly tuberculated and the 
tubercles are large and more marked than usual, and if they ulcerate 
and become deep sores, and finally form, on healing, well-marked 
cicatrices, tertiary syphilis is to be considered the probable cause. 

If, again, we find small nodules under a dusky-red skin, which 
finally breaks down and discharges bloody serum, or pus which in 
burrowing forms discharging sinuses, syphilis of the third stage 
may be regarded as a likely cause. 

The appearance of hard, dark-brown, infiltrated areas in the skin 
may be due to the excessive use of bromine, and as they gradually 
become depressed in the centre closely resemble in some cases the 
nodules of syphilis. 

The roseolous rash of typhoid is sometimes widely distributed and 
almost like measles in appearance; but, as a rule, it is limited to a 
few or many rose spots on the abdomen, chest, or back. These rose 
spots disappear on light pressure, but immediately return when the 
pressure is removed, and are most marked in typhoid fever about 
the seventh to the tenth day of the disease. They may become 
slightly papular. In this connection it should not be forgotten that 
the rose rash of typhoid fever may be so profuse, particularly in 



150 THE SKIN 

persons with a delicate skin, as to resemble scarlet fever; and, 
further, it is to be borne in mind that very rarely scarlet fever and 
typhoid fever may complicate one another. The abdominal symp- 
toms of typhoid fever and the throat symptoms of scarlet fever aid 
in the differential diagnosis. It should be remembered, however, 
that the exhaustion following an attack of scarlet fever may render 
the general appearance extremely like typhoid. In the relapse of 
typhoid fever the rose spots often appear as early as the third or 
fourth day. In typhus fever they are much more plentiful and often 
form petechias. (See chapter on Fever.) 

In Bright' 's disease a roseola often appears over the feet and 
ankles, wrists and hands, and sometimes spreads to the skin of the 
chest and abdomen. Desquamation may take place, but absence 
of febrile movement and the presence of renal trouble render the 
diagnosis easy. This manifestation has not a dangerous import. 

A marked roseola or dermatitis involving the insides of the thighs 
or the scrotum or vulva should give rise to the belief that the patient 
is suffering from a failure to properly pass or retain the urine, which, 
on escaping, irritates the skin. This is particularly apt to result if 
the urine is that of a diabetic. 

It is an interesting fact that in some cases of tuberculous peri- 
tonitis an erythematous rash appears on the abdominal wall around 
the navel. 

An erythematous rash which possesses great importance at 
present in all of the southern parts of the temperate zone is due to 
pellagra. The rash, as a rule, begins on the backs of the hands and 
may resemble an acute or chronic sunburn. It has a shapely defined 
line and usually extends up the forearms. The face, neck, and 
feet may also be involved and ultimately the affected parts become 
pigmented and dry with thinning and atrophy of the skin. In 
grave cases the rash is followed by the formation of bullae and blebs 
associated with hebetude, dyspepsia, vomiting, diarrhea, emaci- 
ation, and death. Often grave mental disorders are present. 
The condition may be constant or remittent and is nearly always 
progressive. 

The presence of a roseola or erythematous rash often indicates 
the untoward influence of some drug, following its external or 
internal use. We find that it very commonly follows the ingestion 
of copaiba, and, as many persons suffering from venereal disease 
take this drug, the physician must use care not to be led into a 
diagnosis of syphilitic roseola. It also follows the use of quinine, 
opium, antipyrine, and many other drugs, such as digitalis and 
chloral. 

The roseola caused by the use of copaiba appears by preference 
on the upper and lower extremities, and particularly on the backs 
of the hands, about the knees and ankles, and on the chest, and it 



ERUPTIONS ON THE SKIN 151 

is often accompanied by fever. Indeed, the eruption caused by 
copaiba may closely resemble a papular syphilide; but its sudden 
onset, itching, and disappearance when the drug is stopped separate 
it diagnostically from the specific disease. 

The roseola following the use of bromide of potassium is, accord- 
ing to Veiel, very rare, and is distributed over the lower limbs. In 
children it may closely resemble measles. 

The roseola or erythema caused by quinine is to be separated 
from that of scarlet fever by the absence of fever, of the scarlet 
tongue and sore throat, and by the fact that there are no prodromes 
or circulatory disturbance except the characteristic evidence of 
cinchonism. In doubtful cases this is still further confirmed by 
analysis of the urine or by the use of the following simple test: 
Observe the disappearance of the fluorescence of the urine caused 
by quinine, after the sodium chloride has been removed by pre- 
cipitation by nitrate of mercury, or after separating the quinine as 
an iodide by the addition to the urine of a solution of two parts of 
iodine, one part of iodide of potassium, and forty parts of water. 
The iodide of quinine can be again dissolved by the application of 
heat. 

A distinct diffuse roseola sometimes follows the use of arsenic. 
Roseola may be caused by the use of salicylic acid and strychnine, 
and a scarlatiniform rash sometimes appears in blotches over the 
face and body in persons who are taking turpentine. 

Roseola also ensues in some persons after the application of sur- 
gical dressings containing iodoform, corrosive sublimate, and car- 
bolic acid, being due either to a local effect of these drugs or to their 
absorption from the dressings. Arnica tincture applied by sprains 
or bruises may produce marked roseola, or even erythematous and 
erysipelatous swelling of the skin, as already stated. 

An important drug exanthem is that caused by atropine, the rash 
produced by it being very like that of scarlet fever, except that it 
lacks the red punctations of that disease. This rash may be asso- 
ciated with a slight rise in temperature and be followed, rarely, by 
desquamation. The face of a child suffering from an overdose of 
atropine is very characteristic. The eyes are bright, the pupils 
widely dilated, and the skin over the malar bones is red, but striking 
lines of pallor reach from the corners of the mouth to the nose. 
There may be active, talkative delirium and very mild convulsions 
from overdoses of atropine, thus making the resemblance to the 
onset of scarlet fever very striking. The brief duration of the rash, 
its lack of punctation, the absence of high fever, and the history of 
the patient having taken atropine or belladonna, all help to make 
the differential diagnosis. 

Roseola, followed by desquamation, has been known to follow 



152 THE SKIN 

the hypodermic injection of mercury. Sometimes the use of blue 
ointment produces a widespread rash resembling measles, and this 
resemblance may be increased by the development of a febrile 
movement. A similar eruption may ensue from the ingestion of 
opium. 

Erythematous rashes, too, frequently follow slight irritation of 
the skin in persons who use chloral. 

Rotheln. — The rash of rubella or rubeola or rotheln (German 
measles) more closely resembles that of scarlet fever in some 
cases than it does that of measles, but it is never as scarlet, is dis- 
tinctly maculated, and only at a distance looks homogeneous. Like 
measles, it is first seen on the face, chiefly about the nose and on the 
upper lip. Close examination always reveals the rash in oval 
patches or crescents, and it lacks the diffused character of the rash, 
the punctation of the skin, the grave systemic disturbance, and the 
throat symptoms of scarlet fever. The rash is not as scarlet as in 
scarlet fever nor as dusky as it is in measles. Further, the febrile 
movement is comparatively slight, and the rash lasts only twelve 
hours or at the most for two or three days. Slight desquamation 
may, however, occur. 

Rotheln, or German measles, is separated from true measles in 
many cases by the marked glandular enlargements, chiefly the 
sublingual, posterior cervical, and inguinal lymph nodes; but this 
is also occasionally true of scarlet fever and sometimes of measles. 
It never presents "Koplik's spots" on the buccal mucous mem- 
brane, but small reddish spots may appear on the soft palate 
(Forcheimer's spots). (See chapter on the Mouth.) The contrast 
between the mildness of the general symptoms and the severity 
of the systemic disturbance in scarlet fever is noteworthy. The 
following differential table devised by Hubbard is useful: 

Scarlet Fever. German Measles. 

More or less severe constitutional Very slight constitutional symptoms. 

symptoms. 

The severity and intensity of the rash The severity and intensity of the 

is in direct proportion to the consti- rash are in inverse proportion to 

tutional manifestations. the constitutional symptoms. 

Enlarged glands, usually following Enlarged post-cervical chain of glands 

onset and evidence of sepsis. like a string of beads early in onset. 

Glands swollen and tender. Glands enlarged, soft, and not tender. 

Confluent scarlet (pink) rash. Non-confluent, dark-red (violaceous) 

rash. 

Rash punctate. Rash macular. 

Onset sudden and more or less severe. Onset sudden but not severe. 

Tongue, milk-coated; later, "straw- Not affected. 

berry," about third day. 

Circumoral pallor. Rash starts about the nose and 

upper and lower lips. 



ERUPTIONS ON THE SKIN 1 53 

Scarlet Fever. German Measles. 

Vomiting. No vomiting. 

Rash appears quickly, spreads rapidly, Rash appears in one part at a time; 

and disappears gradually. appears gradually at other parts, 

fading at place of onset. Covers 

body in about twenty-four hours. 

Rash appears first on neck and about Rash appears about nose and lips. 

clavicular spaces. 
Scarlet rash fades with yellowish shad- German measles rash fades with a 

ing. Leaves skin more or less in- brownish red, then to a light brown, 

jected. and disappears, leaving no mottling 

of skin. 
Desquamation in 12 to 24 days. Desquamation in about 3 days. 

Desquamation in sheets. Squamous Desquamation furfuraceous. 

scales. 
Has more or less severe sequelae. Has none. 

Itching more or less prominent. Not present. 

Measles. — The eruption of measles is very characteristic, and can 
be in most cases easily separated from the other exanthemata by 
close examination. It is roseolous in character, but more dusky 
than that of scarlet fever. It appears about the fourth day of the 
illness in association with catarrh of the mucous membrane of the 
eyes and respiratory tract. Unlike scarlet fever it appears in 
macules first upon the forehead or face, then on the neck, trunk, 
and limbs. The macules, which often coalesce, are arranged in 
crescents which are red, but become somewhat yellowish on press- 
ure. They are slightly raised. There is nearly always to be seen 
some uninvolved skin, the entire surface not being covered as in 
scarlet fever. In some instances in which the eruption is aberrant 
a diagnosis of measles from scarlet fever is admittedly impossible 
until the case has been watched for some days; but the slow onset 
of measles, in which the eruption appears on the fourth day as 
against the first day in scarlet fever, the swollen eyes and nose, the 
puffiness of the face, the catarrhal condition of the mucous mem- 
branes, the curious fall of temperature after the preliminary rise on 
the first day, the short duration of the rash, all aid in the diagnosis 
of measles. The dusky eruption of measles can nearly always be 
found on the pharyngeal mucous membrane. (For the mouth and 
throat symptoms of scarlet fever and measles, see chapter on the 
Mouth and Tongue.) 

So closely may the early rash of smallpox simulate the aberrant 
type of measles as to lead to grave mistakes in diagnosis. Some- 
times an immediate diagnosis is impossible, even by the most 
experienced, but the rash of measles commonly appears on the face, 
therefore this difference, coupled with a history of exposure, the 
gradual development of the peculiar "shot under the skin" sensa- 
tion of variola, and the ultimate distinct papulation, vesiculation, 
and pustulation of smallpox soon remove the doubt from the 
physician's mind. 



154 THE SKIN 

Day of Eruption of the Various Exanthemata. 



Day. 


Disease. 


Area 


First to second day . . . . 


Rotheln or German measles. 


Face first. 




Varicella or chiekenpox. 


Face or trunk. 


Second day 


Scarlet fever. 


Neck and chest 


Third to fourth day .... 


Measles or morbilli or rubeola. 


Face. 




Variola or smallpox. 


Forehead, face, and wrists. 


Fourth to fifth day 


Typhus or ship fever. 


Trunk. 


Seventh to ninth day .... 


Typhoid or enteric fever. 


Abdomen. 



The remembrance that the incubation period of variola is twelve 
days, that of varicella seventeen days, of measles ten days, of 
rubella twenty-one days, and of scarlet fever two to four days, will 
aid the diagnosis if a history of exposure can be obtained. 

A diagnosis between the eruption of measles and variola often 
can be made by stretching the skin between the fingers, when, if it 
be measles, the papule cannot be felt, whereas, if it be variola, it 
persists. This is called the "grisolle sign." (See Acne.) 




Fig. 40. — Smallpox eruption on the seventh day. 

Smallpox. — Somewhat resembling the eruption called acne is that 
which is characteristic of smallpox and chicken-pox. The erup- 
tion of smallpox appears on the second or third day in the form of 
tiny specks, resembling flea bites. These rapidly become papules, 
which have an indurated base, so that they feel as if shot 



ERUPTIONS ON THE SKIN 1 55 

were under the skin (Fig. 40). After about thirty-six hours these 
papules become vesicles, containing a turbid fluid, which speedily 
becomes purulent, forming a pustule. Generally this process of 
maturation takes three days, and, with the development of the 
pus, the so-called secondary fever, which may be even higher than 
the primary fever of invasion, sets in. After a period of eighteen 
to twenty-one days the pustules drop off, having become dried up, 
leaving, if the attack has been severe or the skin delicate, deeply 
pitted scars. The vesicles of variola soon become umbilicated, are 
multilocular, and are difficult to rupture with the finger nail. 
Although the eruption- of smallpox appears on the forehead, which 
is the favorite seat of acne in many cases, a differential diagnosis 
is not difficult, since the grave systemic disturbance, febrile move- 
ment, and rapid involvement of the skin of the limbs speedily 
indicate the true nature of the disease. The early appearance of 
the rash on the hands in variola and backs of the forearms is a 
valuable diagnostic sign, as acne in this part of the skin is prac- 
tically unknown. Then the sudden development of the eruption 
in smallpox is entirely different from the gradual onset even of the 
most intense acne. 

It is not to be forgotten that cases of smallpox develop in which 
the symptoms of systemic disturbances are so mild that it seems 
impossible for true smallpox to be present, and also that acuminate 
syphilide accompanied by febrile movement may develop about 
six or seven months after infection, which may be accompanied by 
such marked systemic disturbance as to resemble smallpox. 

Pustular syphiloderm sometimes resembles smallpox so closely as 
to almost defy an immediate differentiation. The history of syph- 
ilitic infection or of certain syphilitic eruptions, and the absence of 
severe systemic symptoms may aid us, but fever may be present. 
As the pock develops in syphilis it does not become so well umbili- 
cated, nor does it leave deep pits in the skin. 

In some cases a purulent acne of the forehead develops in 
syphilis. I have seen dermatitis due to poison very closely re- 
semble smallpox on the face and hands. 

The separation of variola from measles has already been dis- 
cussed, and it is only in the early papular stage that the former 
disease can be confused with the latter, while the reddened mucous 
membranes and swollen face of the case of measles soon determine 
the diagnosis. The rapid formation of vesicles and the shot-like 
sensation of the eruption show that the rash is not measles. 

Acne of the skin, particularly on the face, is common in young 
persons, is non-febrile, and is often produced by the use of bromide 
or iodide of potassium, or of any preparation containing bromine 
or iodine. That produced by iodine is generally sudden in its onset 
and profuse in its distribution. The base of the pimple is bright 



156 



THE SKIN 



red, the top speedily becomes pustular, and Fournier states that 
it may be hemorrhagic. Stopping the ingestion of the drug speedily 
relieves, or at least decreases, the eruption. The acne due to 
bromine is often very profuse, and the pimples in severe cases 
may coalesce, making sloughs of considerable size with an indu- 
rated base. 

In some persons, generally females, there is developed an acne 
on the face, breast, and back, as the result of taking iron as a tonic. 

In addition to the acne caused by drugs or their compounds, 
mention should be made of the acne and furuncles appearing in 
persons working in paraffin, which is due to blocking of the sebace- 
ous glands. 




«- 






Fig. 41. — Typical vaccine vesicles of a "primary take." Tenth day. 

Vaccinia. — The appearance of the eruption of vaccinia following 
vaccination must be next described. Three or four days after the 
vaccination a single or several papules arise on the scarified surface, 
which by the sixth day are changed into umbilicated vesicles, which 
soon unite and form one vesicle the size of a five-cent piece. This 



ERUPTIONS ON THE SKIN 1 57 

vesicle finally forms a scab, which falls off after the expiration of 
about three weeks from the inoculation. A "good primary take" 
is always surrounded by an areola of rosy red of several inches in 
width. Rarely severe inflammation and sloughing ensue (Fig. 41). 
When the vaccination is a secondary one, the "take," if it occurs, 
often produces no symptoms until the ninth and tenth day, and the 
local lesions are then very mild. 

Chicken-pox. — In chicken-pox the eruption appears on the first or 
second day, and keeps coming out for several days. It is rose- 
colored and occurs as papules, which soon become vesicles. They 
last but four or five days, which is the time that it takes the eruption 
of smallpox to develop, and are usually associated with very mild 
febrile disturbance, the child remaining but little indisposed if 
previously healthy and well cared for and nursed. Unlike smallpox, 
varicella does not become umbilicated unless it grows about a hair 
follicle which holds the centre of the pock, and rarely leaves pits 
in the skin unless the vesicles are picked at by the finger nails. 
Neither do the vesicles become pustules unless infected by picking 
or the child is in a condition of debility. Varicella is separated 
from variola by the absence of severe systemic disturbance, by the 
rash first appearing on the chest and neck instead of the forehead 
and hands, by the presence of other cases of the disease in an 
epidemic, by the repeated crops of the eruption in vaccinia, so that 
several sets of vesicles may be present at one time, and, finally, by 
the fact that it attacks children who have been well vaccinated, 
whereas small-pox does not. The history of exposure is, of course, 
an important point to be investigated. 

The profusion of the eruption is not of diagnostic aid, as it may 
be scant in variola and profuse in varicella. 

In the presence of a papular, pustular, or vesicular eruption of 
the skin it must be remembered that quinine sometimes develops 
these lesions in susceptible persons. In some instances where it 
involves the hands it may indicate that a local effect has been pro- 
duced by working with the drug. 

Impetigo. — An eruption somewhat resembling chicken-pox or 
smallpox is that called impetigo contagiosa, in which there are 
found multiple, flattened or slightly umbilicated, roundish or oval 
vesicles, pustules or blebs, which form after some days dry, yellow- 
ish crusts. It occurs in childhood or early adult life, and is often 
associated with some degree of fever. The areas involved are the 
face, neck, buttocks, hands, and feet. The lesions of the skin are 
larger than in chicken-pox, but often follow this disease. As its 
name indicates, the disease is contagious, and the occurrence of a 
series of cases in close proximity to one another should not mislead 
the physician into a diagnosis of variola or varicella. The eruption 
lasts about two weeks, and Kaposi asserts that swelling of the 



I58 THE SKIN 

submaxillary glands is always present. We can further separate 
impetigo contagiosa from varicella by the localization of its eruption 
to one area, as a rule, by the fact that the eruption becomes bullous 
or purulent, and by the larger size of the vesicle. From smallpox 
we can separate it by the absence of severe pain in the back, the 
grave systemic disturbance, and the secondary fever of that 
disease, accompanied as they are by the smallness of the pox, the 
peculiar odor of the patient, and the history of exposure to variola. 

Eczema in its various forms may appear as the result of the use 
of quinine internally or locally, or of the employment of mercury 
internally or externally. When it arises from the use of iodide of 
potassium, which is very rare, it chiefly affects the scalp and 
scrotum. The development of an eczematous irritation of the skin 
sometimes follows the use of chloral. 

Herpes Labialis is a very constant lesion associated with croupous 
pneumonia, and its development is said to be a favorable sign. It 
is also an important sign for the separation of epidemic cerebro- 
spinal meningitis from meningitis due to other causes, as it is not 
commonly present in the non-epidemic form. It sometimes arises 
as a result of using salicylic acid. 

The presence of herpes rather excludes tuberculosis and typhoid 
fever, in instances in which the diagnosis is doubtful, since it is 
rarely met with in these maladies. 

In the cases of herpes zoster the skin lesion is distributed along 
the course of a nerve and often has its origin in compression of the 
spinal cord, or in such diseases as tabes, spinal meningeal irritation, 
and peripheral neuritis. 

Furunculosis. — The development of recurring crops of boils in 
persons not exposed to paraffin or tar should cause the physician to 
suspect the presence of diabetes mellitus, or at least that there is 
general debility, and particularly an absence of lime salts from the 
system in the proper quantity. 

When the ordinary boil passes into a condition of marked 
induration about its base, with sloughing of the subcutaneous 
tissue and necrosis of the skin, which becomes perforated by the 
openings of several sinuses, we have to deal with a carbuncle or 
anthrax simplex. The disease usually appears on the back of the 
neck, on the back, or the lip. The systemic disturbance is very 
great and the exhaustion profound. The skin covering the area 
involved becomes grayish or bluish black, and then separates as a 
large mass, while the subcutaneous tissue comes away in shreds. 
It is a dangerous disease in all persons, but particularly so in those 
who are already weakened by other disease or excesses. 

Pemphigus. — The development of pea-sized or larger bullae upon 
the skin may indicate the presence of pemphigus, or if there is 
central nervous disease involving the spinal cord and resulting in 



CHANGES IN THE NUTRITION OF THE SKIN 1 59 

trophic lesions similar bullous eruptions may take place. The 
bullae, if they contain dark bloody fluid and are situated upon a 
limb in which there is an abnormally high temperature, aie pe- 
culiarly indicative of central nervous lesions, particularly if there 
is a tendency to dilatation of the capillaries of the skin on slight 
irritation; but if the temperature of the entire body be raised, the 
physician should remember that pemphigus is a disease in which 
there is often marked febrile movement. Sometimes these bullous 
manifestations are followed by gangrene in cases of neuritis or 
other diseases causing trophic lesions, such as myelitis and paretic 
dementia. 

Bullae on the face may follow the ingestion of antipyrine or 
iodine compounds. 

The development of a pemphigus-like eruption in the skin may 
follow the use of salicylic acid or copaiba. 



CHANGES IN THE NUTRITION OF THE SKIN. 

Glossiness of the skin, in which its minute creases become smoothed 
out and it appears unduly shiny, often results from chronic disease 
involving some portion of the nervous system connected with 
the government of nutrition. Very commonly it results from 
peripheral neuritis. In addition to glossiness there are often redness 
and marked thinning or thickening of the cuticle and subcutaneous 
tissues. 

Gangrene of the skin may follow nerve injuries or central nervous 
lesions. Thus it may follow upon division of a nerve trunk, or be 
due to cerebral abscess, in which case the gangrene will be with the 
other localizing symptoms on the opposite side of the body. The 
cerebral form develops suddenly and without the prodromal red- 
ness of bed-sores as seen in prolonged illness. 

A very interesting condition is the so-called spontaneous gangrene 
of hysteria. On the skin, generally of the breast of a young girl, 
a spot develops which feels to her to be hot and burning. The skin 
soon becomes very white, then in a few hours very red and forms a 
wheal. This rapidly becomes dark and bluish black, looking like 
a burn of sulphuric acid, and a slough finally comes away, leaving 
a permanent cicatrix. This condition is very rare. 

The development of gangrene of the fingers and toes sometimes 
follows the prolonged use of bread made from rye which is infected 
by ergot. 

Sometimes gangrene of the skin follows severe attacks of the 
exanthemata in children who are strumous or very feeble, or who 
are syphilitic. 

Ulcers about the base of the finger nails should arouse the sus- 



l6o THE SKIN 

picion of the excessive use of the chloral, unless the patient handles 
some irritant substance in his occupation. (See Raynaud's Dis- 
ease.) 

Gangrene of the skin complicates diabetes mellitus, and may 
involve the scrotum or vulva if the irritation of these parts by the 
urine is constant. More commonly the toes are affected, and there 
is this important differential point, that in the gangrene of old age 
with bad vessels the lesion is usually at the tip of the toe, whereas 
in diabetic gangrene it is frequently about the base of the big toe or 
on the sole or dorsum of the foot. Previous to the development of 
gengrene there are developed bullae and other inflammatory changes 
in the skin which is about to be affected. Kaposi describes a ser- 
piginous form of gangrene affecting the leg in diabetics and a variety 
of tissue break-down in which a dermatitis, followed by ulcers and 
a lupus-like formation, also occurs in diabetes. Perforating ulcer 
of the foot occurs in locomotor ataxia and in paretic dementia. 

Bed-sores may develop whenever by long-continued pressure 
upon any part of the body the local circulation is disturbed, par- 
ticularly if in addition there is general systemic debility from some 
exhausting disease, such as typhoid fever. They also develop very 
speedily in the course of acute transverse myelitis. Under these 
circumstances the sacrum is the area most severely affected. Some- 
times these sloughs have been known to develop as early as six 
hours after the beginning of the attack. Associated with the 
involvement of the soft tissues the bones may break down, and 
cellulitis about the rectum and bladder place the patient's life in 
immediate jeopardy. In hemiplegia, particularly in that which is 
due to cerebellar hemorrhage, bed-sores often form on the buttocks, 
and in paraplegia from other causes than transverse myelitis, upon 
the sacrum. They also appear on the heels, inside of the knees, and 
about the hips in some cases of paraplegia, and in the later stages 
of paretic dementia. 

Speedy sloughing of the skin of the nates rarely occurs in cases 
of intracranial hemorrhage, and is said by Joffroy to be connected 
with lesion of the occipital lobes. 

Raynaud's Disease. — Closely related, yet quite distinct from 
angioneurotic edema, is that condition called Raynaud's disease, 
symmetrical gangrene, or local asphyxia, according to its severity. 
The fingers and toes or the nose, with or without exposure to cold, 
are found to be pale and livid, looking like a hand from which all 
the blood has been removed by the use of an Esmarch bandage. 
The part often feels as if "asleep," and is more or less numb and 
without sensation. To the touch the part is cold and waxy, and it 
does not bleed when pricked. With the onset of these signs there 
are often general chilliness and malaise. Often this manifestation 
speedily disappears, leaving the skin apparently normal; but if it 



CHANGES IN THE NUTRITION OE THE SKIN l6l 

persists, the skin becomes glossy, shrivelled, and looks as if it had 
been soaked in hot water for hours. When the disease is more 
severe the pale waxiness is supplanted by cyanosis until the finger 
tips look as if dipped in blue ink; there is often local swelling; the 
skin is frequently found to be sweating freely and is distended with 
blood. The skin may rapidly separate from the deeper tissues and 
become necrotic in patches or en masse, and the entire tip of the 
ringer, after becoming black, shrivels up into a condition resembling 
dry gangrene, which is separated from the sound skin by a sharp 
line of demarcation. Sometimes small necrotic patches slough out, 
which leave cicatrices telling of the attack. The prognosis as to 
life is not bad. The most interesting complication of the disease 
is paroxysmal hemoglobinuria. 

Scars of the Skin. — Scars of the skin often give us much useful 
information. Indications of early tuberculosis may be found in 
the scars resulting from suppurating cervical glands. In the groin 
such scars may be an evidence of venereal infection, but it should be 
remembered that suppuration of these glands usually takes place 
as a result of chancroids and not from true chancre. It has already 
been pointed out that syphilitic skin lesions often leave scars to 
mark their site. Scars upon the head tell us of possible injuries 
to the brain in suspected traumatic epilepsy, or of falls in epileptics. 
Similarly, other traumatisms in the history of the patient may be 
discovered by scars elsewhere. 

The presence of numerous regularly arranged fine scars on the 
chest or elsewhere may develop the fact that the patient has at 
some time been wet-cupped for some pulmonary or other disease; 
or if the peculiar three-pointed scar of the leech is seen, another 
good evidence of a bleeding is presented. 

When the skin of the abdominal wall exhibits striae or scars 
arranged in parallel series, it indicates that it has been stretched 
very considerably by pregnancy, ascites, or, more rarely, by exces- 
sive corpulence. Sometimes these striae appear on the lower limbs 
in pregnant women or in persons with dropsy. Very rarely they 
may develop on the arms or legs or elsewhere during convalescence 
from some grave disease, such as typhoid fever. 

Sweating of the Skin. — Sweating of the skin, aside from the 
normal and almost imperceptible exhalation of moisture, takes 
place in health as a result of severe muscular exertion, whereby the 
peripheral circulation is increased and the bodily temperature 
raised, or when the body is very heavily clad or exposed to external 
heat in excess. In all these cases the sweating is to be regarded as a 
physiological effort on the part of the body to reduce its temperature 
by increased evaporation from the surface. In disease, sweating 
provides us with very important information in many conditions. 

During the course of fevers which naturally end by crisis the 



l62 THE SKIN 

occurrence of a profuse sweat (generally associated with a fall of 
temperature) gives us the first sign of beginning convalescence, and 
in irritative fevers, or those due to cold and congestion, the early 
production of sweat is decidedly a good omen. The sweat of crisis 
is perhaps most marked in croupous pneumonia. Profuse sweating 
is also a characteristic symptom of relapsing fever, pyemia, acute 
ulcerative endocarditis, advanced tuberculosis, malarial fever of 
the distinctly periodic type, and of typhoid fever and collapse. 
Constant, profuse sweating is marked in some cases of acute 
articular rheumatism, and it is worthy of note that, while 
sweating generally occurs in febrile diseases at a time when the 
temperature is falling, in rheumatism the febrile movement may 
even increase during the sweat. 

Profuse so-called colliquative sweats often occur in sleep in 
debilitated persons without the presence of any febrile movement, 
and are an evidence of profound nervous and vasomotor relaxation. 
Moderate sweating sometimes is seen from similar causes in feeble 
persons taking anything in the food or drink which produces 
circulatory or nervous excitement. 

Localized sweatings occur almost solely in subjects of nervous 
disorder, which is often organic, as in paretic dementia, and some- 
times functional, as in hysteria or Raynaud's disease. They 
depend upon perverted vasomotor influences sent to the glands 
and their supplying vessels in particular areas. Localized sweating 
of one side of the face or neck or chest is often a most important 
sign of a thoracic aneurysm pressing on the cervical sympathetic. 
Bromidrosis may occur in hysteria, or the head may be the only 
part affected in Graves' disease and in migraine. Profuse sweating 
of the head of an infant when sleeping may be indicative of rickets. 
In the toxemia of cholera or of renal disease there may be profuse 
general sweating, which takes the place of the dry and hot skin 
seen more commonly in these conditions. 

The quality of the sweat varies greatly in many persons. In 
cases of deficient renal activity it often smells uriniferous, and 
may even deposit particles on the skin in small white scales, par- 
ticularly on the' forehead and nose. This is called uridrosis. In 
jaundice the sweat may be bile-stained. 

Excessive Dryness of the Skin. — Excessive dryness of the skin 
is seen in grave forms of renal disease, in nearly all acute fevers 
with a high temperature, and in cholera and diabetes, in which 
diseases the dryness is largely the result of drainage of liquids from 
the body. Sometimes after a prolonged dryness of the skin during 
high fever, as soon as sweating begins hundreds of little blisters 
develop, due to retained sweat under the epiderm. These are 
called miliaria or sudamina. 

When the skin is dry and harsh, and the naturally thickened por- 



CHANGES IN THE NUTRITION OF THE SKIN 1 63 

tions have in their folds a peculiar white appearance as if filled with 
meal, diabetes should be sought for. Rarely the physician may be 
deceived by profuse sweating in diabetes, in which disease the skin 
is usually very dry. 

Dropsy and Swelling under the Skin. — Swelling of the skin and 
subcutaneous tissues occurs most frequently as a result of dropsy, 
in which condition the lymph spaces become filled by liquid. The 
skin in the area involved is not only swollen but doughy, or if the 
effusion is very great the skin may be of almost board-like hardness, 
so tensely is it distended. Pressure with the tip of the finger upon 
such an area will result in pitting, and this is one of the more 
important signs separating dropsy or true edema from the swelling 
of acute inflammation, which, while it may be very tense, does not 
pit. Further, the swelling of inflammation is usually localized, 
reddened, and feels hot to the touch, whereas the dropsical swelling 
is more diffuse, is pale, and the temperature of the part is lower 
than normal. 

When the effusion of liquid is limited to one portion of the body 
it is usually called edema or localized dropsy, whereas if the entire 
body is boggy it is designated general anasarca. Dropsy is to be 
differentiated from myxedema by the facts that in the latter disease 
the onset is very slow, the swelling does not pit on pressure and is 
universal and fairly equally distributed over the body, the thyroid 
gland will often be found diseased, the subcutaneous tissues are not 
boggy but resistant, and there is anesthesia of the skin. 

When the subcutaneous tissues are distended by air, instead of 
liquid, they are even less resistant than in dropsy, the swelling is 
usually somewhat localized and does not pit, and the part crackles 
or crepitates on gentle pressure. 

General Anasarca. — The significance of a widely diffused general 
dropsy or anasarca is generally that there is well-marked renal 
disease, and this probability is greatly strengthened if the edema 
of the face be well marked, particularly in the morning on arising, 
disappearing as the day goes on. The skin in such cases will 
usually be quite pale, and an examination of the urine will reveal 
the presence of the signs of nephritis. The next most common cause 
of general anasarca after renal disease is heart disease. When due 
to this cause it will be found that the marked pallor of renal 
anasarca is replaced by cyanosis, and often by engorgement of 
some of the superficial veins, while the physical signs of cardiac 
disease will confirm the diagnosis. Often both cardiac and renal 
lesions are the cause. Care must be exercised that the hemic 
murmur due to anemia does not mislead the physician into a 
diagnosis of heart disease for grave anemia may induce edema. 
General anasarca may rarely arise as a result of a multiple peripheral 
neuritis, and it also occurs as a symptom of beriberi and from 



164 THE SKIN 

the excessive use of large amounts of arsenic. Rarely we find 
general anasarca in cases of advanced cancerous cachexia. 

Local Dropsy.— The most common seat of localized dropsy or 
edema is the feet and legs, particularly about the instep, the ankles, 
and the tibiae. When it is bilateral it is generally indicative of 
cardiac failure or more rarely of renal disease. Nearly always, if it 
be renal, a careful examination will discover edema in other parts 
of the body, although it may be most marked in the feet and legs. 
In many cases the various serous sacs, such as the pericardium, 
peritoneum, and pleurae, will be found to contain more liquid than 
normal, and the tissues generally will be found infiltrated. 

Other causes of edema of the feet and legs are anemia, and 
obstruction to the return of blood from the lower limbs by reason 
of growths in the abdomen pressing upon the iliac veins or inferior 
vena cava. Thus, cancer of the pancreas sometimes causes edema 
of the feet and legs in this manner. Very rarely edema of the 
lower extremities complicates hepatitis or atrophic cirrhosis of 
the liver. Usually such lesions produce ascites alone, or if the legs 
are involved they become so by reason of the pressure of fluid in 
the pelvis during the time that the patient is sitting up or standing. 

Sometimes edema of both legs and feet comes on in persons who, 
though feeble and relaxed, remain standing with little muscular 
movement during many hours in the pursuit of their occupation, 
and in typesetters and salesmen, or in young persons who have 
subjected themselves to excessively severe muscular exercise. In 
other instances, very much more frequently, edema of the feet and 
legs comes on in the course of profound anemia resulting from slow 
hemorrhages or other causes. It is also seen in the cachectic stage 
of cancer, owing to the anemia which is present. 

General swelling of one leg in a puerperal woman is probably due 
to phlegmasia alba dolens, but this affection may also be bilateral. 
Both Herman and Cameron Kidd have each reported a case of 
bilateral phlegmasia alba dolens occurring in a virgin with anemia. 
When phlegmasia occurs in males it is most commonly unilateral 
and a complication of typhoid fever. It is due to thrombosis of 
the left femoral vein, as a rule. 

Dropsy, diffused or localized, in the feet and legs occurs in 
scurvy. 

When the face is edematous the swelling is most marked under the 
eyes, the lower lids of which are particularly puffy in the morning 
and often nearly normal in appearance at night . This form of edema 
is most marked in, and is almost pathognomonic of, renal disease. 
Its only other causes are the excessive taking of arsenic and angio- 
neurotic edema. More alarm should be felt at a slight swelling of 
the face of this character than if the feet are markedly puffed. 
Severe attacks of urticaria may also cause a similar facial state, in 



CHANGES IN THE NUTRITION OF THE SKIN 1 65 

which case, however, there is rarely present any grave disease. 
Sometimes edematous swelling of the side of the face and scalp 
which has been involved in a severe attack of neuralgia takes place. 

When edema of one or both eyelids occurs, with protrusion of the 
eyeball, the swelling extending to the rest of the face as time goes 
on, it forms an important symptom in obscure cases of suspected 
cerebral thrombosis, and is caused by the intimate association 
between the intracranial vessels and those of the face. 

Sometimes edema of the eyelids comes on in neurotic subjects 
and may extend to the forehead. This may be seen in children, 
most commonly about puberty, and is probably the result of a 
neurosis. 

Edema of the upper extremities alone results only from causes 
interfering with the flow of blood, such as are produced by morbid 
growths in the chest, as mediastinal growths, and in cases of aneu- 
rysm. If the swelling of the arms and head is manifested suddenly, 
it may be due to that rare condition in which an aortic aneurysm 
ruptures into the vena cava ; whereas if it develops slowly, it is due 
to pressure by a growth. 

There remain three forms of local edema of some diagnostic sig- 
nificance, namely, that occurring in a limited area over some deep- 
seated suppurative process, as in the skin back of the ear in cases of 
mastoid abscess or thrombosis of the lateral sinuses, that over the 
ribs in cases of purulent exudation into the pleura, and that on the 
thigh in the abscesses which sometimes follow typhoid fever or in 
psoas abscess. 

Myxedema. — When the skin is pale and affected by an edematoid 
swelling, with loss of elasticity, particularly about the face, and 
also in the trunk and extremities, and if this swelling, which 
resembles edema, fails to pit on pressure, the physician should 
remember that myxedema or the cretinoid edema of Gull may be 
present. If in addition to these signs there is a half -idiotic or 
heavy expression of the face, thinness of the hair, a slow and 
labored manner of speech, with thickened, clumsy fingers, the 
diagnosis is made practically certain. The mind in this disease 
perceives or grasps ideas very slowly, and all the functions of the 
body seem torpid. 

There are several other diseases in which great thickening of the 
skin takes place, which cannot, however, be confounded with myx- 
edema. In elephantiasis there is an hypertrophy of skin and sub- 
cutaneous tissues which is confined to some particular region of the 
body and arises from local circulatory disturbance in the blood and 
lymph vessels. The skin is very hard, so that the leg, if affected, 
feels like a solid mass of wood. The disease most commonly affects 
one of the legs, rarely both, and the scrotum. In both myxedema 
and elephantiasis the process develops very slowly. 



1 66 THE SKIN 

Scleroderma. — When the skin is dotted with irregular patches or 
streaks, which may be elevated or tightly stretched, or if the entire 
skin is thickened and infiltrated without inflammation, covered 
with thin scales, or possesses a plaster- like appearance, the physician 
should recognize these symptoms as indicative of scleroderma. If 
in addition to these signs there is a fleeting pitting of the skin on 
pressure, and it cannot be pinched into a fold, the diagnosis is 
confirmed. Sometimes the skin if sclerodermatous, seems bound 
down by tense cords or bands of retracted connective tissue to the 
tissues beneath, and in rare instances even the tendons, muscles, 
fasciae, and joints may be involved. When the part affected is 
about a joint and immobility is present, the impaired movements 
of the joint usually depend upon the stiffening of the skin, but in 
some cases the disease results in atrophy of the deeper tissues. 

The affection just described is to be separated from edema neona- 
torum, a condition arising in prematurely born children. Within 
a few days after birth there is discovered a pallid, cold condition of 
the buttocks, thighs, legs, and arms. The parts speedily become 
edematous and livid blue. Finally, the edema may become very 
marked and the skin tense in consequence. Intense drowsiness is a 
characteristic of the disease. Death commonly ensues, but recovery 
may ocur. While the color of the skin may be identical in edema 
neonatorum and sclerema neonatorum, the former affection lacks 
the stiffness of the jaw and other joints, and the pitting on pressure 
is marked. As scleroderma does not occur before the first year, it 
can be excluded from the diagnosis. 

Adiposis Dolorosa.— No better place can be found in which to 
mention that condition in which irregular and numerous masses of 
fat are to be found in the subcutaneous tissues of middle-aged 
persons, usually women; these masses are more or less painful, 
and occur in the body and extremities. The skin itself is not 
altered. Dercum first described this state and gave it the name 
of adiposis dolorosa. 



SENSATION IN THE SKIN. 

It is important to remember that the sensibility of the skin may 
be divided into four parts, namely, its tactile sense, its pain sense, 
its thermic sense, and its sense of pressure. Any one of these 
senses may be perverted or in abeyance without the others being 
affected, and it is noteworthy that, while corresponding areas of 
the skin in all individuals have practically identical sensibilities, 
each part of the skin has a sensitiveness of its own, so that while 
in some parts the slightest touch is felt, in others severe irritation 
must be produced to cause such a result. These differences have 



SENSATION IN THE SKIN 



167 



been carefully studied by many observers, the most thorough being 
Weber, who has found that the average ability to appreciate separate 
points brought in contact with the skin is about as follows: at the 
linger tips points can be separated at from 2 to 3 mm., on the lips 
4 to 5 mm., on the tip of the nose 6 mm., on the cheeks and backs 
of fingers 12 mm., and on the forehead 22 mm. The skin on the 
neck separates points at 34 mm. ; that on the forearm, on the lower 
leg and back of foot at 40 mm.; on the chest at 45 mm.; on the 
back at 60 mm.; and on the arm and thigh at 75 mm. 

If tests be frequently repeated in a single individual, the ability 
to separate the points increases with training. Care should always 
be taken that the pressure on both points is equal, applied simul- 
taneously, and that the points are equally sharp. 

In testing tactile sensibility, not only should points be used, but 
also objects. Often single points may be applied without any 
abnormal manifestation, and, in 
some cases of disease, the skin, 
which seems devoid of sense on 
ordinary touch, is found to be ex- 
cessively hyperesthetic if the hand 
is drawn lightly over it. 

The best apparatus for testing 
tactile sensibility is the esthesio- 
meter of Carroll, which is a pair 
of double-pointed compasses con- 
nected by a graduated scale. (See 
Fig. 42.) 

The ability to distinguish pain- 
giving and thermal applications is 
most acute in the normal skin of 
the hands, in which tactile sense 
is also most acute. 

The methods by which we test 
the pain sense are several, but 

chiefly by pricking the skin, more or less deeply, with some sharp- 
pointed instrument, such as a pin, or by pinching the integument. 

The thermal sense is studied by applying bodies which are hot or 
cold against the skin, such as a cold knife, a small piece of ice, or a 
test-tube which contains very cold or hot water. In all such tests 
the physician should use both hands simultaneously. With one 
hand he should apply his instrument to the suspected area, and with 
the other a similar instrument to the area known to be healthy, in 
order that an actual comparison as to the sensations may be noted 
by the patient. Thus the face may be used as the normal area in 
a spinal lesion, and the skin of the arms as a control surface in a 
lesion involving the legs. The eyes of the patient should be blind - 




Fig. 42. — Carroll's esthesiometer. 



1 68 . THE SKIN 

folded, and if tactile sense is being tested the instrument must be 
of the same temperature as the body. 

Closely connected with the subject of tactile sense is what is 
known as stereognosis, or the ability to recognize objects by 
contact and grasp. By this means healthy persons are able with- 
out looking at an object to judge of its character, and in the blind 
this sense is very highly developed. Manifestly the entire sensory 
apparatus must be intact for stereognosis to be performed, since 
any interference with the sensory system will produce that condi- 
tion which is known as "astereognosis." Not only does stereog- 
nosis involve the tactile sense but also muscle sense, since it is by 
the grasping of the object that information concerning it is gained, 
as well as by its coming directly in contact with the hand. At the 
present time the discovery of astereognosis in a patient has not 
very definite clinical significance, so far as localization of the lesion 
producing this condition is concerned, but when astereognosis does 
not depend upon a disease of the sensory nerves, it depends upon 
involvement of the cerebral cortex, in the middle third of the 
posterior central convolution and in the adjacent part of the 
inferior parietal lobule. Of course, it is possible for a lesion in the 
sensory fibres of the internal capsule to cause astereognosis; but a 
lesion of any size in this region will usually produce signs of motor 
paralysis, owing to the juxtaposition of the motor and sensory 
fibres. 

The duty of the physician in all cases is to determine first whether 
the disorder of sensation is functional , or organic, and, if the latter, 
where the lesion producing the symptoms is situated. 

Disturbances in the sensation of the skin may arise from func- 
tional disease, or organic disease involving the peripheral nerves, the 
sensory tracts in the spinal cord, similar tracts in the lower parts 
of the brain, and, finally, the subcortical or cortical parts of the 
cerebrum itself. 

The sensory pathway or the afferent fibres pass upward, starting 
with the peripheral sense organ in the skin, or elsewhere, and after 
forming part of the nerve trunk and entering the ganglion on the 
posterior root, enter the spinal cord by what is called the posterior 
root, which is shown in Fig. 43. 

The posterior root enters the cord in three sets of fibres; one of 
these, the one lying nearest the posterior median fissures, is com- 
posed of coarse fibres and is called the median bundle, and passes 
obliquely into the lateral part of the column of Burdach. As soon as 
they have entered this column they turn at right angles and run 
upward for some distance, thereby helping to form the column of 
Burdach. Some of them also run downward a short distance. 
Some of these fibres also enter the column of Goll. 

The second set, near the side of the cord, goes directly into the 



SENSATION IN THE SKIN 



169 



gray matter of the posterior horn through the substance of Rolando, 
and the third set, nearest the side of the cord, enters the cord very 
superficially, and, turning at once at a right angle, goes upward to 
form Lissauer's zone. Hence they pass upward chiefly in the 
column of Goll (posterior median) to the medulla oblongata. 
Before reaching the medulla, however, the column of Goll ends in 
the gracile nucleus and the column of Burdach in the cuneate 
nucleus. 



Posterior root rf 




1 "*l 

1 s 1 

i & ft 


Hi 




Crossed- 


^ 1 


pyramidal 
tract 




Fig. 43. — Columns of the cord. (Gray.) 



These nuclei which have received the fibres of the two sensory 
columns give origin to fibres which pass to the brain. They sweep 
forward to the front of the central canal of the medulla and decus- 
sate at a higher level than the motor tracts. A great majority of 
these fibres pass upward to the brain, but some pass forward, and 
finally join the restiform body on the posterior aspect of the medulla. 
Those which pass upward from the so-called fillet pass into the 
cms cerebri, in that part of it called the tegmentum, and thence 
into the posterior part of the posterior limb of the internal capsule, 
whence they spread out in the corona radiata to the occipital lobe 
and temporosphenoidal lobes. 

The two chief manifestations of perverted sensibility in the skin 



170 THE SKIN 

are anesthesia and hyperesthesia, and the minor ones are pares- 
thesia or numbness, tingling and formication, and analgesia, or the 
failure to feel pain. Whatever the cause of these symptoms may 
be, the history of the patient and his general symptoms should be 
carefully studied when examining these signs, as frequently a diag- 
nosis is possible with them alone as guides. 

Anesthesia. — Anesthesia of the skin is indicative of a very large 
number of conditions arising anywhere in the sensory apparatus. 
In other words, anything which interferes with the transmission of 
an impulse to the perceptive centres in the brain may be its cause. 
Of the functional causes, the most frequent is hysteria, and the 
presence of cutaneous anesthesia in a female should always arouse 
a suspicion of its being due to this cause. Rarely is it seen in hys- 
terical males. The organic causes of anesthesia of the skin are 
cerebral hemorrhage, cerebral tumor, hemorrhage in the pons or 
tumor of the pons, hemorrhage in the cord, tumor of the cord, mye- 
litis (transverse), locomotor ataxia, syringomyelia, insular sclerosis, 
cerebrospinal meningitis, spinal meningitis; compression of the cord 
by vertebral caries, by fractures, by dislocations; and hemorrhage 
into its membranes. Additional causes are pressure on the posterior 
nerve roots by reason of caries and growths, inflammation of the 
nerves (neuritis), injuries to the nerves by blows, pressure, or 
cutting, and, finally, by paralysis of the nerve endings from cold 
or the action of drugs. 

Anesthesia, according to its area of distribution, may be divided 
into hemianesthesia, crossed anesthesia, bilateral anesthesia, irreg- 
ular but complete anesthesia, and partial anesthesia. 

Hemianesthesia occurs most frequently as a result of hysteria, 
next from a lesion of the posterior part of the internal capsule, 
and more rarely from spinal injuries or growths in the cord of a 
unilateral character. 

The hemianesthesia of hysteria involves, as its name implies, 
one side of the body, and is usually universal on that side, except 
that here and there may be patches of hyperesthesia or tenderness, 
dotted-like oases in the midst of the absence of sensation. This 
anesthesia is often unaccompanied by motor paralysis, and its 
area is separated from the opposite side of the body by a sharp line 
of demarcation, which runs along the middle of the trunk and face. 
The presence of such a well-defined line of separation in a young 
woman is of great significance. The anesthesia is generally absolute, 
and severe injury may be done to the skin in some cases without 
the patient feeling it; but, notwithstanding its degree, it is a note- 
worthy fact that the anesthesia may transfer itself to the opposite 
side of the body with great suddenness, and equally suddenly 
return to its former site. In a great majority of cases, for some 
unexplained reason, the left side is the one affected by anesthesia, 



SENSATION IN THE SKIN 171 

and hyperesthesia on the opposite side increases the contrast which 
exists between it and that in which sensation is lost. (See Hyper- 
esthesia.) In some cases of hysterical hemianesthesia the paralysis 
of sensation involves the nerves of special sense; and loss of smell, 
taste, and hearing, and impairment of sight may ensue on the same 
side. The visual changes are so characteristic that they practically 
decide the character of the case when they are discovered in any 
instance of doubtful diagnosis; they consist in reversal of the 
color fields, and there is a great limitation of the visual field. 
Hemianopsia due to hysteria is so rare as to be denied an existence 
by most authorities, but Lloyd and de Schweinitz have seen a case. 
Generally the loss of vision on the anesthetic side is a total one for 
both sides of. the eye in hysterical blindness. (See chapter on the 
Eye.) Nearly always in hysterical hemianesthesia a spot can be 
found over the shoulder which is not anesthetic. The age of the 
patient, the sex, the general expression of the face, and the history 
of the illness, associated, as is frequently the case, with some or all 
of the hysterical symptoms detailed farther on in this chapter, will 
generally decide the diagnosis in favor of hysteria. 

A form of hysterical hemianesthesia very apt to lead to an error 
in diagnosis is that seen in persons who have suffered from infantile 
cerebral paralysis with the resulting deformity (a disease not char- 
acterized by sensory disturbances), but who have in later life 
superimposed upon the old picture of disease, that of hysteria with 
this sensory manifestation. 

Hemianesthesia when not hysterical is nearly always due to an 
organic lesion in the posterior part of the hinder limb of the internal 
capsule on the opposite side of the brain from the anesthesia, and 
the additional symptoms which sometimes accompany it depend for 
their existence upon whether the lesion is large enough to involve 
not only the fibres from the cutaneous areas, but also the motor 
fibres. Nearly always the area destroyed is sufficiently large to 
result not only in hemianesthesia, but also in loss of motion on the 
same side. The loss of sensation in such a case is rarely as complete 
as in hysteria, becoming less marked near the median line of the 
body, and the sole of the foot and palm of the hand are often not 
affected. In rare instances, however, the hemianesthesia of cap- 
sular disease may be absolute and universal, or, more rarely still, 
occur in patches, thereby closely resembling the anesthetic areas 
seen in hysteria. 

Hemianesthesia may also be produced by a large lesion of the 
cortex in the occipital, temporal, and parietal lobes, in which case it 
will involve the side of the head as well as the trunk, and will be 
associated with such definite evidences of apoplexy or injury that 
the diagnosis will be readily made. If it is widespread, all the 
special senses will be involved. 



172 THE SKIN 

Sensory disturbances of the skin are more frequent in softening 
of the brain than in hemorrhage into the brain, and most commonly 
are associated with subcortical, rather than cortical lesions. 

In this connection it should be remembered that the irregularity 
of distribution of the lesions in disseminated sclerosis may cause a 
hemianesthesia, partial or complete. 

Anesthesia resulting from tumor of the brain occurs in about 20 
per cent, of the cases, and may be unilateral and confined to the 
paralyzed side, or appear as an isolated symptom without motor 
paralysis. When of the latter form it is often associated with lesions 
in the neighborhood of the fissure of Rolando, and in tumors 
involving the posterior parietal region and the posterior part of the 
internal capsule. 

Autopsies and experiments show that hemianesthesia may arise 
from a lesion in the optic thalamus, but such an occurrence is very 
rare. 

A very important and essential factor in making the diagnosis 
that the anesthesia is cerebral in origin is the history of the begin- 
ning of the attack, which has been sudden if due to hemorrhage, 
embolus, or thrombus (see Hemiplegia), but sudden anesthesia in 
young women is in the vast majority of cases hysterical. 

An important point to be noted in the diagnosis of cerebral anes- 
thesia is the fact that the reflexes are preserved, though the patient 
may not feel the touch or painful impression; that is to say, irrita- 
tion of the skin causes movement in the arm or leg, not by any 
intention of the patient, but owing to the fact that the sensory 
centres in the cord receiving an impulse cause the corresponding 
motor centres to send out impulses which reflexly contract the 
muscles. 

Unilateral anesthesia associated with motor paralysis, both being 
somewhat irregular in their distribution, may be due to a lesion, 
such as a tumor in the pons or medulla oblongata, but death so 
commonly ensues soon after the apoplexy that the symptom is often 
overlooked or cannot be developed when this accident is the cause. 
Further, the discovery of such anesthesia does not positively localize 
the lesion in the pons, for we do not know much about the course 
of the sensory fibres in this part. If, however, the area supplied 
by the trifacial nerve, namely, the face, is anesthetic, and symptoms 
named are present, then it is fair to assume that the trouble lies in 
the pons and has involved the nucleus of the fifth nerve. (See 
Anesthesia of the Face.) 

Anesthesia of Irregular Distribution or confined to one limb may 
result from cerebral or spinal lesions, or be due to a neuritis, of 
which I shall speak farther on. If it is a mono-anesthesia from 
cerebral disease, which is very rare, the anesthesia is most marked 
at the distal part, and gradually fades off as the trunk is approached. 



SENSATION IN THE SKIN 1 73 

It is evenly distributed, so far as circumference is concerned, and 
has no sharp line of demarcation. 

When such an anesthesia is due to spinal disease the cause may 
be tumor of the spinal cord, the symptoms depending in their char- 
acter on the area involved; but in any event the upper border of the 
area involved is sharply outlined and a constriction-band sensation 
is often present. 

The irregularly distributed form of anesthesia due to hysteria has 
the same general peculiarities of distribution as are seen in hemi- 
anesthesia from spinal cord disease, and in its symmetrical form it 
superficially resembles the anesthesia due to multiple neuritis. Thus, 
in the hand the area of anesthesia may be that covered by a gauntlet 
glove, in the foot that covered ordinarily by a sock, the line of 
normal sensation being present just above the place to which these 
protections usually extend. 

There is no sensory loss in chorea but only in hysterical chorea. 

Crossed Anesthesia of the limbs and face — that is, anesthesia of 
one side of the body with anesthesia of the opposite side of the face 
— can only occur in lesions involving the upper part of the pons in 
such a way that the fibres of the trifacial are diseased on one side, 
and the path for sensory impulses of the other side of the body is 
also destroyed. (See chapters on the Face and Head, and on Hemi- 
plegia.) 

Partial hemianesthesia, with partial hemiplegia on the opposite 
side, may occur from lesions on one side of the spinal cord, and if 
high up, involve a large part of the trunk and lower limbs. (See 
chapter on the Feet and Legs, part on Myelitis.) These cases have 
been explained by a theory of Brown-Sequard, which has recently 
been doubted owing to the studies of Mott and others. Thus, 
until recently it was considered as proved that sensory impulses 
entering the cord crossed to the opposite side almost at once, at 
least in greater part, passing to the lateral columns in front of the 
pyramidal tract, and that a very small number entered the pos- 
terior columns, while a few ascended in the gray matter. The 
studies of Mott seem to prove that the reverse is the case, and that 
the greater part of the sensory impulses do not cross the cord, 
only a few fibres passing to the opposite side on entrance. He 
believes that the main pathway for heat and cold sensations is in 
the gray matter, while the tactile pathways are in the posterior 
columns, although it is possible that some few isolated fibres may 
exist in the lateral columns and that these cross in the cord about 
the level of entrance. 

Bilateral Anesthesia. — Anesthesia of hysterical origin involving 
both legs, and sometimes the lower part of the trunk on both sides, 
may occur, and, aside from the typical signs of hysteria in general 
which distinguish it, may be discovered by the fact that in hysteria 



174 THE skin 

the failure of sensation does not involve the skin of the genitals, as 
it does in organic lesions producing somewhat similar symptoms. 
In addition it will be found in hysteria that a V-shaped piece of 
skin over the sacrum is not anesthetic. Anesthesia of this variety, 
corresponding in the sensory organs to what we call paraplegia in 
the motor apparatus, is practically never produced by a cerebral 
lesion, and, if not hysterical in cause, must be spinal; but it is much 
more rare than is motor paralysis in these parts from lesions in the 
spine. When it does ensue from spinal causes motor paralysis 
will in the great majority of cases be found associated with it, at 
least to some extent. To express it concisely, the characteristic of 
a typical spinal anesthesia is that it is bilateral and usually involves 
both sides quite symmetrically; that motor paralysis is generally 
associated with it; that the reflexes are greatly perverted; and that 
trophic changes may be present as a result of an involvement of 
the trophic cells in the anterior cornua coincidently with the disease 
of the sensory parts of the cord. 

The diseased conditions of the cord which result in symmetrical 
anesthesia of the skin of the legs and trunk are, first and most 
prominent, locomotor ataxia; second, myelitis; hemorrhages, tumor 
of the cord or its membranes, meningitis, or injuries which cause 
pressure on the sensory tracts by producing fracture of the vertebrae 
or dislocation. Very rarely, however, a lesion of the pons may so 
result. 

Anesthesia of the lower portions of the body and legs not sym- 
metrical in distribution occurs in the later stages of locomotor 
ataxia, and is usually preceded by forms of paresthesia. (See 
Paresthesia.) The anesthetic areas are most marked in the 
soles of the feet and about the malleoli, according to Belmont. 
In other words, blunting of sensibility is seen in nearly all cases of 
tabes dorsalis late in the disease. In some cases the sense of touch 
is preserved and the sense of pain lost (analgesia), while in others 
the opposite condition is present. Again, we find loss of tactile 
sense and pain sense without loss of heat and cold sense, and vice 
versa. A very characteristic sensory symptom of tabes is the delay 
in the recognition of an irritation of the sensory nerves, so that if 
the patient be blindfolded and then pricked with a pin he will not 
make an exclamation or draw his foot away for several seconds. 
In other instances the patient complains of repeated pricks when 
only one has been given, or, when asked the number of points 
pricking him, states that there are four or five instead of the one 
really present. If, in addition to these sensory disturbances, we 
find Romberg's symptom (see Legs), Argyll-Robertson pupils 
(see Eye), and loss of patellar reflex (see Reflexes), and a number 
of the other diagnostic peculiarities of tabes, the decision as to the 
cause of the anesthesia is easily made. 



SENSATION IN THE SKIN 1 75 

An important early diagnostic sign of locomotor ataxia is the 
development of areas, unilateral or bilateral, of diminished sensi- 
bility. This is particularly apt to be found in the areas supplied by 
the mid-dorsal nerves (level of fourth intercostal space.) They are 
very constant symptoms. When the disease is advanced the anes- 
thesia extends down the inside of the arms and forearms. The 
sense should be tested by a warm finger tip applied to the skin 
in a very gentle manner. 

Bilateral anesthesia of the character just discussed, as caused by 
locomotor ataxia, may also occur as a result of acute or chronic 
myelitis. The first change under these circumstances is a mere 
obtunding of sensitiveness, which gradually deepens until loss of 
pain sense, pressure sense, and, lastly, complete anesthesia is 
developed. Loss of reflex activity in the legs is developed in 
direct proportion to the destruction of the motor and sensory 
nerve tracts in the cord. The predominance of motor par- 
alysis, the fact that the lower limbs are both involved, and the 
absence of the characteristic symptoms of locomotor ataxia all tend 
to make the diagnosis certain, while the absence of the pains of 
tabes and of the other signs of that disease still further excludes its 
presence from the case. Further than this, the myelitis creeps up 
the cord, involving new areas, and new parts of the skin become 
anesthetic. An important point, too, in regard to the anesthesia 
of acute myelitis is this, namely, that while in the upper extremities 
the loss of sensation and motion is associated, so that both functions 
are lost in the same area, in the lower extremities these two functions 
are not lost in the same areas. Thus, myelitis of the lumbar enlarge- 
ment in its lower part is accompanied by anesthesia of the gluteal 
area and motor paralysis of the anal muscles; and, again, anesthesia 
of the gluteal region, the back of the thigh, and the back of the calf 
is associated with loss of power in the muscles that move the foot, 
while in lesions of the upper part of the lumbar segment the anes- 
thesia involves the thigh, the inner side of the leg, and the foot, in 
association with paralysis of the quadriceps extensor and deeper 
muscles of the thigh. (See chapter on the Feet and Legs, part on 
Myelitis.) 

The development of sudden bilateral anesthesia, which is accom- 
panied by severe pains of a tearing or burning character, creeping 
rapidly up the body, is indicative of acute hemorrhage into the 
spinal membranes, or, if little or no pain is present, it may be due 
to that very rare lesion, hemorrhage in the cord. In either case 
motor paralysis is present. Anesthesia, or the milder perversions 
of normal sensibility of the skin, may be present in cases of com- 
pression of the cord by caries, and by spinal curvature, tumors, 
or aneurysms producing erosion. Sometimes while tactile anes- 
thesia is complete in these cases, severe pain is constantly suffered 



176 



THE SKIN 



(anesthesia dolorosa), and this is often the case, according to Wood, 
in cancer of the spine. 

Slight anesthesia, retardation of the transmission of sensory 
impulses from the skin, and perversion of temperature sense may 
be rarely developed late in the course of Friedreich's ataxia. 

Partial anesthesia of the skin of the trunk and arms of a bilateral 
character, associated with progressive muscular atrophy, scoliosis, 
and trophic lesions in the skin, points strongly to syringomyelia. 
The loss of pain and temperature sense is usually the first symptom, 
this sensory dissociation being very characteristic of the disease. 
The areas of anesthesia are best shown in Fig. 44. 




Fl ^o1^ng^ s r of Chart : ■ 3 ^»^'««<W, llllll 



Thermo- Anaesthesia 
and Analgesia 

Tactile Anaesthesia,, and areas in which the patient's answer to tests of tempera- 



ture showed reversal 8 8 8 \Hot-Cold!, m a case °f syringomyelia. (Dercum.) 



Localization of the Spinal Lesion. — Having considered the general 
spinal causes of anesthesia of the skin, it yet remains to determine 
what part of the cord is involved by the pathological process; and 
this is, fortunately, possible, chiefly through the very accurate and 
noteworthy studies of M. Allen Starr, Thorburn, and Head, not to 
mention collateral ones of great value by Horsley and many others; 
but the field is only partly covered, and some of our uncertainties 
depend upon lack of knowledge as to the course of the sensory fibres 
in the cord. 



SENSATION IN THE SKIN 



177 



Roughly, we may state that disease of the cervical cord generally 
produces disturbances of sensation in the arms, hands, and ringers; 
disease of the dorsal cord, disturbances in the sensation of the 
back and trunk, which may radiate into the thighs; and disease 
of the lumbar cord gives rise to these symptoms in the legs and 
feet. 

Again, it is to be remembered that, as a rule, in a transverse 
lesion of the spinal cord the anesthesia begins at a level which is 
three or four inches below the lesion in the cord (Horsley and 
Gowers) ; this being due, as proved by Sherrington, to the fact that 
each area of skin is supplied by three nerve roots whose peripheral 
filaments overlap one another. 



8th cervical and 1st dor 
sal segment at 7th ver 
tebra. 



Lumbar enlargement o 
cord at 10th dorsal v 
tebra. 



End of cord at 2d lumbar ) 
vertebra. J 



Cauda equina 




1st to 7th cervical 
vertebra. 



1st to 12th dorsal 



vertebra. 



1st to 5th lumbar 



vertebra. 



1st to 5th sacral 
vertebra. 



Fig. 45. — Showing the surface areas of the back corresponding approxi- 
mately to the areas of the spinal cord supplying the trunk and limbs. 



For the ready study of the subject the cord has been separated 
into segments corresponding with the vertebrae covering it. The 
areas of anesthesia produced by spinal injury or disease are best 
described by Starr's well-known article and diagrams, from which 
we quote. In this connection the reader should refer to the tables 
on pages 93 and 94, showing the localization of the functions of 
the segments of the spinal cord. (See chapter on the Legs and 
Feet.) 



12 



i 7 8 



THE SKIN 



The anesthetic areas included in zones I and II in Fig. 46 are due 
to a lesion involving the conus medullaris and the fourth and fifth 
sacral segments of the cord. These zones include the peritoneum, 
the posterior part of the scrotum in males, the vagina in females, 
and the mucous membrane of the rectum. Anesthesia in zone 
III is due to lesion of the third, fourth, and fifth sacral segments, 
and includes a large part of the buttock and the upper part of the 
thigh, posteriorly, in a triangular space. Zone IV is practically 





Fig. 46. — Areas of anesthesia in lesions at various levels of the spinal cord 

from sacral V to lumbar II. (After Starr.) 

I. Sacral v. IV. Sacral 1. 

II. Sacral iv. V. Lumbar v. 

III. Sacral in. VI. Lumbar in. 

VII. Lumbar 11. 



an enlargement of zone III in every direction, particularly toward 
the popliteal spaces, and is probably due to a lesion in the first and 
second sacral segments; but this needs confirmation by autopsy, 
as Starr points out. Zone V includes all the first four zones just 
named, and extends down through the popliteal space in a band- 
like shape; after it passes this space it descends the outer side of 
the leg and foot, sometimes ending at the ankle, sometimes at the 
sole or the three outer toes and half the next toe. Such an area 
indicates a lesion involving all the segments of the sacral cord, and 



SENSATION IN THE SKIN 



179 



extending into the lumbar cord to the fifth lumbar segment. Zone 
VI is caused by a lesion extending to the third lumbar segment, and 
when it is present the anesthesia covers the back of the thighs and 
legs and also the front of the thighs, except in an area which extends 
from above downward along the shin, sometimes to the foot, as in 
Fig. 46. If the foot is involved, the lesion in the lumbar cord is 
probably above the third lumbar segment. Zone VII, which is 
larger than all, follows a lesion in one of the four lumbar segments — 
that is, all but the first. The line of anesthesia, Starr tells us, is 
lower in front than behind. When the abdominal wall is involved 
in the anesthesia the first lumbar segment is probably diseased. 





w 




Fig. 47. — Areas of anesthesia from lesions at various levels of the spinal 
cord from the second dorsal to the fifth cervical. (After Starr.) 

The areas of the anesthesia of the abdomen corresponds very 
closely to the levels in the cord, if we allow for the space, already 
mentioned, of two to three inches for the interlacing anastomosis 
of the nerve fibres of the posterior roots. 



l8o THE SKIN 

They are about as follows, according to Thorburn : When the anes- 
thesia is as high as the anterior superior spine of the ilium, the lesion 
is at the twelfth dorsal vertebra; if at the umbilicus, at the eleventh 
and twelfth dorsal vertebrae; if up to the lowest floating rib, the 
whole eleventh dorsal vertebra; if one to four inches above the 
umbilicus, the ninth and tenth dorsal, and perhaps part of the 
eighth dorsal vertebra; if as high as the nipples, the fourth dorsal 
vertebra; and if to the third rib, the lesion is as high as the second 
dorsal vertebra. 

Starr has also given us, in another paper than that already quoted, 
equally good ideas of the areas of anesthesia occurring above those 
just described (Fig. 47). When the anesthesia extends to the 
arms and is found upon the inner side of the arm and forearm, 
reaching to the wrist, but not to the hand, and also involves a small 
zone on the extensor and flexor surfaces of the arm and forearm, 
the second dorsal region is the site of the lesion. If the anesthetic 
area includes the ulnar side of the hand, the palmar and dorsal sur- 
faces of the same, and the little finger, and extends in a narrow 
strip up to the axilla on both the anterior and posterior surfaces of 
the arm and forearm, the lesion is probably at the level of the eighth 
cervical vertebra. When the zone involved extends to the middle 
of the central figure on the palmar and dorsal aspects, and runs up 
the centre of the forearm and arm, the seventh cervical area is dis- 
eased. Again, when the remaining skin of the hand up to the wrist 
and a narrow strip of skin up the forearm and arm on both surfaces 
to the axilla is affected, the lesion is at the sixth cervical vertebra, 
while anesthesia of the forearm and arm on the outer surface as 
high as the deltoid insertion indicate the fifth cervical vertebral 
area in trouble. Lesions higher than this usually produce death 
before it is possible to test sensibility. 

Neuritis as a Cause of Anesthesia. — Anesthesia of the skin in any 
part of the body may be due not only to cerebral or spinal lesions, 
but also to neuritis or inflammation of the nerve trunk, or to some 
injury which impairs its functional activity by pressure, bruising, or 
cutting. As a rule, loss of sensation from neuritis occurs late in the 
disease, hyperesthesia or paresthesia being the earlier manifestations ; 
but in some cases these are absent, and anesthesia begins at once. 
The characteristic of such an anesthesia is that it is confined to 
the area supplied by the affected nerve, although the presence of a 
multiple neuritis may produce such a universal anesthesia by involv- 
ing all the nerves that this sign is masked. While a mono-anesthesia 
may be due to other causes, notably hysteria, it is in the great 
majority of cases due to neuritis. The signs of an anesthesia due 
to neuritis are loss of motion and sensation, tenderness on pressure 
over the nerve trunks supplying the affected areas, later on trophic 
changes in the tissues of the part, with the development of reactions 



PLATE V 




Cervical Roots are represented by the letter C; Dorsal Roots by the letter D. 
and Lumbar Roots by the letter L. (Chart after Head.) 



SENSATION IN THE SKIN 1 51 

of degeneration and pain in the involved nerves or parts supplied 
by them. 

Toxic peripheral neuritis producing anesthesia may arise from 
poisoning by arsenic, lead, alcohol, or mercury, from septic states 
of the body, and from the infectious diseases, particularly diph- 
theria, influenza, and typhoid fever. 

That due to the mineral poisons has in each case certain differen- 
tial points of importance. The anesthesia of arsenical poisoning is 
more marked than in lead poisoning, in which condition it is often 
almost absent, and the lower extremities are very apt to be involved, 
whereas in lead poisoning, as is well known, the nerves of the arm 
are particularly susceptible. (See chapter on the Arms and Hands.) 
Arsenical neuritis may also produce pigmentation of the skin. In 
alcoholic neuritis the temperature of the anesthetic areas is often 
subnormal and there are nearly always mental disturbances repre- 
sented by delusions. In mercurial poisoning, shaking, like paralysis 
agitans, may be present. An analysis of the motor symptoms in 
all these cases is important, and the discovery of any one of these 
poisons in the urine, with the history of the patient, generally makes 
the diagnosis possible. 

Diphtheritic neuritis is quite common, and in 50 per cent, of the 
cases in which it occurs sensibility is lost or disturbed in the areas 
supplied by the involved nerves. 

Great care is needed in all cases of neuritis lest the mistake be 
made of diagnosticating the condition as one of locomotor ataxia, 
when in reality it is pseudotabes. 

It has already been stated that in neuritis the area of anesthesia 
is that supplied by the affected nerve. For this reason we can deter- 
mine what nerve trunk is affected by studying the area of anesthesia, 
always remembering, however, that the sensory fibres of the nerves, 
particularly in the hands and feet, anastomose so freely with those 
of adjacent nerves that the area of the anesthesia may not be exactly 
that supplied by the nerve involved; or, in other words, the presence 
of loss of power in a region supplied in health by a nerve which has 
been divided is constant, but very often sensation is not disturbed, 
even though the divided nerve be the sensory as well as the motor 
supply to the part. 

It is well to remember also that sensory disturbance of the skin 
following injuries of nerves are often not nearly so great as the 
motor disturbance, even where there is no sensory transmission by 
anastomosis, and where they are present they usually disappear, 
more rapidly than the motor loss, as recovery takes place. 

The following facts are, therefore, of diagnostic interest. If the 
anesthesia is found to be due to a neuritis and to involve the palmar 
surface of the thumb, fore and middle fingers, the median nerve 
is probably the one at fault (Figs. 48 and 49), and the area ma}' 




Fig. 48. — Area of anesthesia from injury of the median nerve. 
Palmar surface. 




Fig. 49. — Area of anesthesia from injury of the median nerve. 
Dorsal surface. 




Fig. 50. — Area of anesthesia in injury of the ulnar nerve. Dorsal surface. 




Fig. 51. — Area of anesthesia from injury of the ulnar nerve. Palmar 

surface. 



184 



THE SKIN 



even include in rare instances the backs of these fingers at their 
bases and the half of the third finger nearest the thumb. When 
there is disturbance of sensation in the ulnar side of the ring finger 
and in the skin of the little finger, there may be ulnar neuritis (Figs. 
50 and 51). (See also chapter on the Hands.) The nerve supply 
of the skin of the entire upper extremity is well seen in Fig. 52. 





Fig. 52. — Cutaneous nerve supply of the trunk and upper extremity. (Fowler.) 
sa. Supraclavicular nerve, iid. Second dorsal, ps. Posterior branches of the 
spinal nerves, li. Lateral branches of the intercostal nerves, ai. Anterior 
branches of the intercostal nerves. c. Circumflex nerve. m. Intercostal 
humeral, w. Nerve of Wrisberg. i'cb. Internal cutaneous branch of mus- 
culospiral nerve, ecb. External cutaneous branch of musculospiral nerve. 
icb. Internal cutaneous nerve. mc. Musculocutaneous nerve. R. Radial 
nerve, u. Ulnar nerve. M. Median nerve. 



The development, of sensory disturbances in the feet, resulting 
from neuritis, is as follows: When there is perverted sensation of 
the inner side of the foot from the tip of the big toes to the heel, 
and thence up the inside of the calf to the knee, the nerve involved 
is the long or internal saphenous. When the dorsal surface of the 
foot has its cutaneous sense disturbed the nerve involved is the 
musculocutaneous, a branch of the external popliteal. Disturbance 



SENSATION IN THE SKIN 



185 



of sensation on the outer side of the foot and calf indicates failure 
of function in the external saphenous, which is composed of the 
cutaneous branches of the external and internal popliteal nerves. 
Disturbed sensation on the posterior surface of the calf also indi- 
cates trouble in the external saphenous nerve and communicans 
peronei, while when the sensation of the skin of the heel is dis- 
turbed the plantar cutaneous nerve, a branch of the posterior 
tibial, is involved (Fig. 53). 



ic 



Fig. 53. — Cutaneous nerve supply of the lower extremity. 11. Ilio-inguinal. 
iil. Second lumbar nerve, gg. Genitocrural. EC. External cutaneous, mc. 
Middle cutaneous, ic. Internal cutaneous, is. Internal saphenous, ss. Small 
sciatic, ep. Branches from external popliteal, es. External saphenous, mcs. 
Musculocutaneous, pt. Branches of posterior tibial. (Modified from Gerrish.) 



In the skin of the thigh the anterior surface is supplied by the 
middle cutaneous nerve, which is a branch of the anterior crural ; 
on the inner side by the internal cutaneous, also a branch of the 
anterior crural; and on the outer side by the external cutaneous, 



1 86 THE SKIN 

which arises from the second and third lumbar nerves. Laterally 
the external cutaneous gives the supply. Posteriorly the small 
sciatic gives the nerve supply to the skin. 

Anesthesia of the greater portion of the skin of the thigh, except 
in a narrow strip on the back part and in the area supplied by the 
internal saphenous nerve, often occurs as the result of paralysis of 
the anterior crural nerve, arising from pelvic tumors, psoas abscess, 
and vertebral disease. 

Facial Anesthesia and its diagnostic meaning are still to be con- 
sidered. When it occurs it indicates that the fifth nerve, or its 
nucleus, is involved. 

If the area be that of the forehead, the upper eyelid, the conjunc- 
tiva, and the nostril, the ophthalmic branch of the fifth nerve is at 
fault, and the lesion is probably at the sphenoidal fissure or within 
the orbit, and reflex winking of the eye on touching the lid no 
longer takes place because the conjunctiva is anesthetic. 

If the skin of the upper part of the face is anesthetic, the superior 
maxillary branch is involved ; and if the skin of the temporal region 
and that of the jaw and the under lip are anesthetic, the inferior 
maxillary branch is diseased. When both of these branches are 
paralyzed there is probably a tumor of the superior maxillary bone ; 
and if the entire area of the three branches is anesthetic, the Gas- 
serian ganglion may be the part affected, and this will be accom- 
panied by trophic changes in the anesthetic parts. The most com- 
mon cause of anesthesia of the trifacial is, however, neuritis. 

Romberg makes the following differential statement: 

(a) The more the anesthesia is confined to single filaments of the 
trigeminus, the more peripheral the seat of the cause will be found 
to be. 

(b) If the loss of sensation affects a portion of the facial surface, 
together with the corresponding faucial membrane, the disease may 
be assumed to involve the sensory fibres of the fifth pair before they 
separate to be distributed to their respective destinations; in other 
words, a main division must be affected before or after its passage 
through the cranium. 

(c) When the entire sensory tract of the fifth nerve has lost its 
power, and there are at the same time derangements of the nutritive 
functions in the affected parts, the Gasserian ganglion, or the nerve 
in its immediate vicinity, is the seat of the disease. 

(d) If the anesthesia of the fifth nerve is complicated with dis- 
turbed functions of adjacent cerebral nerves, it may be assumed 
that the cause is seated at the base of the brain. 

Other Disturbances of Sensation than Anesthesia. — The other 
disturbances of sensation of the skin than anesthesia, which are 
usually subjective rather than objective, are paresthesia, hyperes- 
thesia, and analgesia. 



PLATE VI 




Showing the Distribution of the Cranial Nerves, particularly the Fifth. 
(Modified from Arnold.) 

III. Branch of oculomotor to inferior oblique. V. The Gasserian ganglion, composed of the 
fibers of the sensory root of the nerve. (The plate would seem to indicate that the three branches 
of the nerve arise from this ganglion, but they do not, for the motor fibers do not enter the 
ganglion, but join the sensory fibers in the third branch, after they leave the ganglion.) XII. 
The hypoglossal nerve. 



SENSATION IN THE SKIN 187 

Paresthesia. — Numbness, tingling, or burning — is seen in nearly 
all cases in which anesthesia ultimately develops as a result of 
organic lesions. When a patient complains that he cannot feel the 
contact of clothing about his feet and legs, or that the feet when he 
walks feel as if wrapped in some thick material, or as if he were 
walking on moss, or that the soles of his feet feel as if they were 
numb and at the same time tickled by ants walking over them, the 
characteristic sensory disturbance of the skin seen in locomotor 
ataxia is present. 

Often there is tingling or numbness of the fingers, particularly of 
the ring and little fingers, and a sensation as if a girdle were about 
the patient in common. These are the subjective disturbances of 
sensation in tabes dorsalis, and, as they are often the earliest mani- 
festations of the disease, possess great diagnostic importance. The 
objective sensory perversions consist in the discovery by the physi- 
cian, when studying the sensibility of the skin, of areas of anesthesia, 
analgesia, and hyperesthesia which are usually bilateral. Belmont 
has stated that we also find these areas in spinal syphilis, either 
on one or both sides. Numbness, tingling, and formications affect- 
ing the skin are also often early symptoms of brain tumor in the 
area supplying the affected part, and this possibility is increased 
if there is associated spasm. The actual objective sensibility of the 
skin may be preserved for some time after these symptoms appear, 
or it may be impaired almost at the outset, owing to the involvement 
of all or part of the sensory tracts in the cord. Similar symptoms 
are often seen in the early stages of myelitis. They are very fre- 
quently seen after injuries to nerves, and severe tingling in its acute 
variety occurs when the " funny bone" of the elbow is knocked 
against an object, owing to bruising the nerve. It is also seen in 
cases of aconite poisoning, and when the hands have been exposed 
to carbolic acid. Paresthesias are also frequently seen in cases of 
neurasthenia. 

Perversions of sensation in the skin sometimes take a curious 
form, as, for example, that known as allochiria, in which a sensory 
impulse in one hand is referred by the patient to the opposite hand. 
This is seen in tabes dorsalis, myelitis, multiple sclerosis, and hys- 
teria. In other cases, as in paralysis agitans, this perversion takes 
place in the form of failure to distinguish heat and. cold, and subjec- 
tive sensations of extreme heat are felt. The part affected may 
actually have its temperature raised several degrees. 

Magnan asserts that a sensation as if a worm or bug were 
crawling under the skin is indicative of cocaine intoxication. 

Very closely associated with the numbness of hysteria or neuras- 
thenia, and lying between functional and organic, disease of the 
nerves, is that condition called acroparesthesia, or waking numb- 
ness. This state is usually seen in women past middle life, but 



1 88 THE SKIN 

may occur in men. On waking in the morning marked formication 
and numbness of the fingers are present, which usually pass off as 
the day progresses, but as the condition develops they may last 
all day. While there is no anesthesia, strictly speaking, the dis- 
turbed sense of touch renders sewing or performing any small act 
with the fingers almost impossible. These sensations may be 
confined to the area of one nerve, as the ulnar, or involve all the 
skin of the hands, or more rarely of the feet. General nervous 
excitability is usually associated with the local manifestations. 
Sometimes the scalp may be the area involved. 

Acroparesthesia is to be separated from the sensory disturbances 
of hysteria by its irregular outline, for generally in the latter disease 
the areas are distinctly outlined, by the fact that the hysterical 
condition is usually unilateral, and by the absence of the charac- 
teristic general hysterical symptoms. From organic disease it is 
separated by the absence of the signs of neuritis about to be de- 
scribed, and by the absence of tenderness, pain, and loss of power. 
From cerebral or spinal disease it is separated by the absence of 
symptoms produced by lesions in these parts, and by the facts that 
in both these lesions there is paralysis of motion in association with 
the sensory disturbance, and in the case of spinal lesions the symp- 
toms are usually in the legs, while acroparesthesia generally 
manifests itself in the hands. 

Closely associated with paresthesia, if not an actual form of it, 
is the "girdle sensation;" that is, the patients feels as if a tight belt 
were strapped around a limb or the trunk. This is seen as a promi- 
nent symptom in locomotor ataxia, myelitis, and tumors of the cord 
or its envelopes. When the lesion is in the lower cervical or dorsal 
region the sensation is in the chest or abdomen; but this relationship 
between the growth and the sensation of constriction is not always 
constant. (See chapter on the Feet and Legs.) 

Hyperesthesia of the skin is an important symptom of both 
hysteria and neurasthenia, and its discovery in association with the 
peculiar symptoms which occur in the former morbid state confirm 
a diagnosis most positively. The most important and curious of 
these hyperesthesias are the so-called hysterogenous zones, or, in 
other words, areas involving the skin and subcutaneous parts, which 
possess great sensitiveness, and which, when pressed upon, cause in 
many cases convulsive seizures of the hysterical type. Not only is 
this true, but in addition it is a noteworthy fact that after the 
nervous disturbance produced by this means is set in motion, a 
second pressure on the hysterogenous zone may arrest the seizure. 
These zones commonly exist over the ovaries, in the groin, about 
the periphery of the mammary glands, or upon the spine in the 
lumbar or dorsal region. (See chapter on Pain.) 

The hyperesthesia due to neurasthenia is to a great extent spinal 



SENSATION IN THE SKIN 1 6g 

in character, but the skin of the rest of the back, particularly over 
the great muscles on each side of the spine, may also be involved. 
Often the neurasthenic patient, or one who has phosphaturia, will 
complain that in brushing or combing the hair, pain or extreme 
sensitiveness is developed upon the scalp, and there may be tender 
areas on the chest. These areas in neurasthenics can hardly be 
confused, even by the careless, with the hyperesthetic zones of 
hysteria, and the personal history and characteristics of the 
individual aid still further in separating the two conditions. 

Hyperesthesia, aside from that seen in hysteria and neurasthenia, 
occurs in peripheral neuritis and locomotor ataxia, the skin of the 
back being particularly tender in the latter disease, and the exces- 
sive sensitiveness is frequently seen in a zone extending a little 
above the anesthetic areas of transverse myelitis, this hyper- 
esthetic area being soon rendered anesthetic by the progress of the 
disease. Hyperesthesia in the skin of the limbs is also rarely seen 
in myelitis, and when there is motor paralysis of one side and sen- 
sory paralysis of the other it is commonly found on the side on 
which motion is lost. A condition of excessive dermal hyperesthesia 
is also present in cerebrospinal meningitis, in which disease it is 
often a very early symptom. It usually appears first in the legs, 
then in the hands and arms, and, finally, the skin of the face and 
head become involved. 

Hyperesthesia is considered by some authors to be, when found 
in association with other characteristic symptoms, almost pathog- 
nomonic of brain tumor. It may be found on the scalp, over a 
large part of the body, or in the part which is paralyzed. It is 
also found during the convalescence of typhoid fever and in re- 
lapsing fever. It also appears in the paralyzed side of persons 
suffering from hemiplegia, in the area supplied by a nerve suffering 
from neuralgia, particularly that of a migraine type, in the scalp 
of persons suffering from gout, and in the same area in women 
about the time of the menopause. 

The hyperesthesia of chronic alcoholism may be both dermal and 
deep, and is well marked along the course of the peripheral nerves, 
particularly where they emerge from deeper structures. It is also 
seen in the neuritis of lead and arsenical poisoning. 

Hyperesthesia occurs, often associated with skin eruptions, in 
that very rare condition called chronic leptomeningitis. 

General Tenderness of the skin or deeper tissues is quite fre- 
quently seen in cases of rickets and scurvy, the child crying 
whenever it is moved, as if sore and tender, and tender spots 
often appear over the ribs in cases of pleurisy. 

Sometimes in a neurotic girl about the time of puberty, or in a 
woman, one breast becomes exceedingly painful and tender, and 
the skin of the part becomes so hyperesthetic that the slightest 



190 THE SKIN 

touch causes pain. The whole breast is, moreover, tender, and 
movement of the arm may be impossible, owing to pain thereby 
caused in the gland. This hysterical breast can be separated from 
the painful breast due to inflammation by the general diffuse 
character of the swelling, the failure to outline any distinct mass, 
the neurotic character of the patient, and her age. 

Increased sensibility of the skin may follow the use of opium or 
ergot, and is met with in the course of, or as a sequel of, influenza, 
and in some cases of profound anemia. 

In some cases hyperesthesia is an early sign of the onset of non- 
tuberculous leprosy, and will generally be found in the course of 
the ulnar or sciatic nerves in such cases. 

A very interesting fact from a physiological and diagnostic point 
of view is that disease of the internal organs or viscera often pro- 
duces areas of hyperesthesia or tenderness upon the skin, which 
may in future be used to aid in the localization of the lesions. This 
subject has been well studied by Head, from whose researches much 
information may be derived, but the results of which will have to 
be confirmed in many cases before they can be used as diagnostic 
guides. (See chapter on Pain.) 

Pain in the skin is very various in its manifestations, and nearly 
always is due to functional nervous trouble. Duhring has noted 
a boring sensation in some cases. It should direct the physician's 
attention to the possibility of hysteria or tabes dorsalis. 

Pruritus, or intense itching of the skin, may be due to contact 
with some irritant, but its presence, if persistent, particularly if 
widespread or near the genitals, should always raise a suspicion of 
diabetes mellitus, or chronic lead poisoning, or gout, or chronic con- 
tracted kidney. Very rarely opium may produce a pruritus, and 
jaundice is nearly always accompanied by some itching. Pruritus 
about the anus is often due to piles, gout, and diabetes. 

Finally, one important point is to be remembered, viz., we cannot 
attempt to make a general diagnosis merely from a study of the 
areas of anesthesia or other perverted sensibility of the skin in any 
case. The results obtained from studies of the sensation of the 
skin are only to be used as additions to the motor and other symp- 
toms, which will be found discussed under the chapters on the 
Limbs. 



CHAPTER VII. 
THE TONGUE, MOUTH, PHARYNX, AND OESOPHAGUS. 

The general appearance of the tongue — Its coating — Its appearance in poisoning 
— Fissures and ulcers of the tongue — Eruptions on the tongue — Atrophy 
and hypertrophy of the tongue — Paralysis — Tremor and spasm of the 
tongue — Tonsillitis — Diphtheria — Pharyngitis — Disease of the oesophagus. 

THE TONGUE. 

The appearance of the tongue is recognized as indicative of the 
general condition of the patient, and is a valuable diagnostic aid in 
many diseases other than those associated with disorder of the 
gastro-intestinal mucous membrane. In examining this organ the 
physician should take note of the condition of its surface, its shape 
as it lies in the mouth or is protruded, and the character of its move- 
ments. He should also see that it is well protruded, and examine 
the back of it more than the tip, as the latter is the part giving the 
least information. 

Before discussing the precise appearance of the tongue in the 
various disorders in which it becomes altered in appearance it is 
well to remember that its surface is covered by mucous membrane, 
which differs in various parts. The epithelium is scaly and rests 
upon the corium or mucosa. The mucosa also supports many 
papillae, which are thickly distributed over the anterior two-thirds 
of the tongue on its upper surface. These papillae give the peculiar 
roughness which is so characteristic of this surface, and occur in 
three forms, namely, the circumvallate or large papillae, the fungi- 
form or mediate, and the filiform. The circumvallate are only 
eight or twelve in number, and are arranged at the back of the 
tongue in the shape of the letter V, with the point toward the root 
of the organ. The fungiform papillae are scattered freely over the 
tongue, mostly at the sides and tip, and appear as deep-red emi- 
nences, the bases of which are smaller than their free extremities. 
Their epithelial covering is very thin. The filiform papillae, which 
cover the anterior surface of the tongue, are very minute, and 
arranged in lines corresponding in direction with the two rows of 
the circumvallate papillae. From their apices project many line, 
filiform processes which are of a whitish tint, owing to the density 
of the epithelium of which they are composed. There are, in 



I92 THE TONGUE, MOUTH, PHARYNX, AND OZSOPHAGUS 

addition, many simple papillae which cover the surface between the 
peculiar ones already described. The fungiform papillae are those 
seen most commonly in cases of disease, for they become large and 
prominent, and because of their red color show through the coating 
as red dots. 

The appearance of the surface of the tongue varies greatly even 
in health according to the condition of its mucous membrane and 
the epithelium covering it. The most common alterations in its 
appearance are due to mere superficial coatings or fur, which con- 
sist of dead epithelial cells, microorgansims or many kinds, and 
abnormally shaped living epithelium. Small particles of food may 
also be present. Butlin believes that the coating is chiefly due to 
microorganisms. 

The question as to how characteristic of a particular disease 
any one coating or fur may be has been warmly discussed. Some 
have gone so far as to assert that the coating of the tongue is 
not indicative of any state in particular, while others, of whom 
the author is one, are convinced that, while an absolute diagnosis 
of disease in other organs cannot be based upon the appearance 
of the tongue, great aid can be gained by its study. There are, 
however, very few conditions of the coating of the tongue which 
are pathognomonic of any one disease, since the coating is pro- 
duced by the local conditions of the mouth rather than by the 
disease itself. 

Taking up for consideration the various forms of coating, we find 
that the area at the base between the circumvallate papillae is 
always somewhat coated even in the best of health, and that in 
disease the heaviest coating is generally found in this region, while 
the tips and sides, even in these diseases in which the coating is 
heaviest, are generally fairly clean. This is in part due to the 
character of the epithelium in different parts, and to the fact that 
the tip and sides are generally scraped clean by the movements of 
the tongue. Further, it should be remembered that the develop- 
ment of coating, aside from digestive derangements, depends chiefly 
on three factors: First, immobility of the tongue, so that it is not 
kept clean by rubbing; second, mouth breathing, whereby the 
surface becomes dry and less easily cleansed; and, third, fever, 
which not only dries the surface of the tongue, but interferes with 
salivary secretion. Additional local causes are a decayed or ragged 
tooth or follicular tonsillitis, which infects the lingual epithelium, 
lack of cleanliness, and habits, such as smoking. In the last class 
of patients, the smokers, a heavily coated tongue in the morning 
is very common. 

The tongue of the typhoid state, and of typhoid fever in particu- 
lar, is quite characteristic, because the prolonged illness, the great 
exhaustion, and the general apathy of the patient all conspire to 
produce a peculiar coating on this organ. Early in the disease the 



THE TONGUE 1 93 

surface of the tongue may be more or less foul, resembling the coat- 
ing associated with biliousness, in that the back part is coated 
evenly and with a paste; but very soon a characteristic sign appears, 
namely, that the tip of the tongue and its edges become red, and the 
coating becomes most marked on each side of the median fissure, 
which increases in depth from before backward. The tongue also 
becomes narrow instead of broad and flabby, as it is in biliousness, 
and is drier. If the attack be mild, this condition may remain until 
convalescence is established; but if the disease runs a severe course, 
the coating becomes very heavy, more dry, rough, and brown from 
exposure to air and medicine. The furred appearance becomes 
almost shaggy at the back portion, and the drying proceeds until 
the underlying epithelial layer is cracked and fissured so that tiny 
exudations of blood add to the lingual discoloration. The reddened 
edges become dusky in hue, and may be cracked and fissured also. 
The tongue is very slowly protruded on request, partly from mental 
apathy, partly from feebleness and because its surface is so stiffened 
that to move it is difficult. It is equally slowly withdrawn for 
similar reasons, and while protruded is often markedly tremulous. 
Toward the close of the attack the tongue cleans off through 
exfoliation of the dead epithelial accumulation, and this is a favor- 
able or unfavorable sign according to whether the remaining surface 
is red and moist or dusky and dry. Sometimes these characteristic 
coatings do not appear, the tongue being brown and rough all 
through the disease. The heavily coated dry tongue just described 
is, however, rarely seen in those cases of typhoid fever which are 
treated by cold bathing. 

A small, triangular patch devoid of coating is often seen at the 
tip of the tongue in relapsing fever. 

In uremia the tongue is often dry, brown, cracked, and furred. 
The patient, if conscious, complains of a foul taste and the breath 
may smell like stale urine. 

In biliousness the tongue is coated almost uniformly by a whitish- 
yellow, pasty coat, extending from back to tip and side to side. The 
tongue is broad and flabby, and sometimes indented by the teeth, 
while the breath is foul and heavy. A similar tongue is seen in 
severe tonsillitis, except that it seems even more foul and less yellow 
in tint. Similarly in jaundice of the acute catarrhal type we have a 
coating still more yellow in some cases, because, as Fothergill 
asserts, the coat has been stained by the taurocholic acid eliminated 
by the salivary glands. The circumvallate papillae are often promi- 
nent and stand above the coating, which is easily removed on 
scraping. 

A broad, white, heavily coated, moist tongue is often seen in 
acute articular rheumatism, becoming dry if the fever is high and 
the attack prolonged, 
13 



194 THE TONGUE, MOUTH, PHARYNX, AND OESOPHAGUS 

The white tongue of a person who takes large mounts of milk is 
generally not smooth but rather rough and pasty in appearance. 
If the tongue be suffering from an attack of thrush (Saccharomyces 
albicans), the white coating will consist of irregular white masses of 
the growth, which, if in great numbers, often coalesce and make a 
fairly even surface. The soreness of the mouth, the local heat, the 
salivation, and the age of the person — generally a young child — 
render the diagnosis easy, 

A grayish diphtheritic-looking coating of the tongue, occurring 
in adults, may be due to the growth of various forms of mycoses. 
Thus a fine network of leptothrix in threads and tufts often spreads 
over the tongue, particularly in the region of the circumvallate 
papillae. The growth may be quite dark in color, but it is sepa- 
rated from the exudate of diphtheria by microscopic study and the 
absence of systemic disturbance. 

Sometimes on examining the tongue of a child we find that it is 
broad and flabby and covered by a gray coating, which is smooth 
and fairly moist. Scattered throughout this coating are patches in 
which the coating and epithelium have been shed, leaving red spots 
with sharply defined edges, which spots are said to be "worm-eaten" 
in their appearance — that is, to have the irregular outline of the 
marks on a worm-eaten leaf. In these areas are to be seen enlarged 
and reddened fungiform papillae. Such a tongue is typical of what 
has been called, by Eustace Smith, " mucous disease" a condition 
in which there exists a more or less marked chronic catarrhal process 
in all the mucous membranes. If, on the other hand, there is a 
comparatively light coating, dotted irregularly by bright red spots 
which are not raised above the surface, but are very numerous, and 
the patient is a child, the diagnosis may be made of acute or 
subacute gastric catarrh. 

The so-called "strawberry tongue" is one in which the organ is 
entirely denuded of coating and superficial epithelium, while the 
fungiform papillae are swollen or enlarged and stand out prominently. 
This appearance of the tongue is seen commonly in scarlet fever, 
but is not, as has been thought, pathognomonic of that disease. 
The fungiform papillae in the strawberry tongue of scarlet fever 
are, however, particularly prominent and erect. 

When the tongue is excessively furred or rough in appearance, 
the coating is due to abnormally long and projecting papillae 
covered by an excess of living and dead epithelial cells; it may 
denote grave disease of the viscera, but in rare instances possesses 
no diagnostic importance, unless coupled with other symptoms. 
This tongue is sometimes seen in scrofulous children in whom 
strumous manifestations are marked. 

Should the tongue be denuded not only of coating, but, in addi- 
tion, of its normal epithelium, so that it appears dry, hard, and 



THE TONGUE 1 95 

harsh to the touch, it denotes, as a rule, grave and advanced disease 
of an exhausting nature, such as renal, hepatic, or gastric disorder 
about to cause the death of the patient. Sometimes this condition 
is seen in advanced phthisis, diabetes, or gastric carcinoma, and is 
of evil omen. 

When the tongue is bereft of epithelium, beefy and red looking, 
elongated and narrowed, and shows a peculiar roundness when 
protruded, severe disease of the abdominal organs, such as dysentery, 
or hepatic abscess, or carcinoma, will often be found, or, in some 
cases, this condition develops to add to the discomfort of cases of 
advanced pulmonary tuberculosis or acute peritonitis. This tongue 
is sometimes called the " parrot tongue." 

In this connection the point should be noted that dryness of the 
tongue in the presence of grave disease is always an evil omen, and 
returning moisture of the tongue a favorable one. 

Unilateral coating of the tongue may be due to a decayed or 
ragged tooth, or to hemiplegia, which prevents that side of the 
tongue from being cleaned through movements. Hillow and 
Fairlie Clark both assert that morbid conditions of the second 
division of the trifacial nerve cause unilateral coating, and that 
abnormalities of the third division do not produce these changes 
as we would expect. 

The coating of the tongue is often so stained by extraneous sub- 
stances as to be entirely changed in appearance. If the coating be 
black, the color may be due to the ingestion of iron, of bismuth, 
charcoal, ink or blackberries, mulberries, cherries, or red wine. 
In very rare cases it is black, not from the growth of a fungus, 
as has been thought, but from overgrowth of the epithelium with 
the deposit of a black pigment of unknown origin. Usually this 
brownish-black discoloration is confined to the middle of the 
tongue. The affected surface is often rough, due to the enlarged 
papillae, and the edges of the spot are less black than the centre. 
In professional tea tasters the tongue may be orange-tinted. 

The coating may be stained brown from the chewing of tobacco, 
from licorice, nuts, prunes, or chocolate, and yellow from the 
ingestion of laudanum or rhubarb. 

The color of the tongue itself, aside from discoloration of its 
epithelium, is an important diagnostic aid. It is exceedingly pale 
in all forms of anemia, particularly those due to lack of hemoglobin, 
such as chlorosis or acute anemia from hemorrhage, and in per- 
nicious anemia, when well advanced, it has a remarkable pallor. 
It is livid and cyanotic in cases of pulmonary disease interfering 
with oxidation of the blood, or in cardiac disease with similar 
difficulty and when very large doses of coal-tar drugs have been 
taken. 

Purple spots, which may be almost black, may be present on the 



I96 THE TONGUE, MOUTH, PHARYNX, AND OZSOPHAGUS 

tongue in Addison's disease. Sometimes they are bluish black, 
and always well denned and even with the surface. 

Very rarely the tongue is discolored by infarcts, blood stains, 
and bruises. 

When the tongue has its edges dotted with yellowish patches of a 
slightly elevated character, the condition is xanthelasma, and the 
liver wi]l often be found to be disordered. 

In cases of poisoning by corrosive sublimate the tongue presents 
a most characteristic appearance, for it is white and shrivelled, and 
the papillae at the base are unusually large. 

When sulphuric acid has been swallowed the tongue has a parch- 
ment-like appearance, is at first white and then gray or brownish 
gray, and finally is covered by a black slough, which as it separates 
leaves a swollen, excoriated patch. In nitric acid and chromic acid 
poisoning the tongue is shrivelled and lemon yellow in color, as 
it is when hydrochloric acid has been swallowed. The tongue of 
carbolic acid poisoning is very characteristic indeed, for the mucous 
membrane is shrivelled and puckered into folds. The spots where 
the acid has touched it are brownish if impure acid has been swal- 
lowered, or white if the pure acid has been taken. In the course of 
a few hours this spot becomes surrounded by a red zone, and finally 
becomes dark brown or black in the centre. After oxalic acid is 
taken the tongue may be covered by a thick white coat and looks 
as if it had been scalded. Caustic potash and soda soften the mucous 
membrane, so that it is pulpy and easily detached, and looks 
pearly, red, or yellow in hue. When ammonia is swallowed the 
color is white, but superficial edema may make it pearly in appear- 
ance, and acid nitrate of mercury renders it very red. Cantharidal 
poisoning produces large lingual blisters and sores. 

Aside from the coating and color of the tongue, its surfaces should 
be examined to discover fissures, cracks, ulcers, sloughs, and swell- 
ings. The tongue is often seen to be superficially and irregularly 
fissured in old persons, particularly in those who have used large 
quantities of strong alcoholic drinks or strong tea, or who have 
chewed tobacco incessantly for many years. The fissures cross each 
other in every direction, although the central fissures which run 
longitudinally is generally deepest and longest. If the furrows are 
very deep, they may indicate the early stages of what Wunderlich 
has called dissecting glossitis, which in turn may be due to syphilis, 1 
although, as a rule, the fissures of the tongue due to syphilis are 
deepest at the edges of the organ, and are due to pressure by 
irritation from the teeth or to ulceration with subsequent cicatriza- 
tion of small syphilitic nodules or gummas. The cervical glands 
are rarely involved in such cases. If only one ulcer is present it 

1 This is denied by Demarquay and doubted by Butlin, 



THE TONGUE 1 97 

may be chancre, which will have the peculiar Hunterian hard base, 
and, in such a case, the cervical glands will probably be enlarged. 
As deep syphilitic ulcers heal, sclerosis of the tongue may develop. 
An epithelioma may also have an indurated base with secondary 
glandular enlargement. Lingual ulcers may also be present as the 
mucous patches of syphilis, or be due to wounds from the teeth, a 
broken pipe-stem, or a fork. When these become chronic their 
separation from those due to syphilis and tuberculosis is practically 
impossible on superficial examination. Sometimes an ulcer of the 
tongue is due to epithelioma; but if this is the case, the patient will 
probably be past thirty years of age. 

Multiple ulceration of the tongue may be due to tuberculous dis- 
ease, which is very rarely primary, but secondary to its presence 
elsewhere. The sores are often stellate in shape, and there is 
always swelling of the cervical lymphatics, whereas in multiple 
syphilitic ulceration of the tongue the glands generally escape. The 
diagnosis between tuberculous ulcer and that due to epithelioma is 
more difficult, since in both diseases the cervical glands are 
involved. Both are more common in men than in women. The age 
of the patient, the presence of tuberculous disease elsewhere, and 
the absence of induration point to tubercle. The tuberculous ulcer 
is not surrounded by much inflammation, is covered by grayish, 
purulent mucus, and may contain bacilli of tubercle, and is often 
associated with tuberculous nodules which have not broken down. 

Ulcers of the tongue may also be due very rarely to lupus. 

A very similar tongue is seen in a tropical disease with intestinal 
disorder called sprue or "psilosis." A hypersensitive herpetic erup- 
tion appears on the tongue and mucous membrane of the mouth, 
which leaves large areas devoid of epithelium, while sinuous furrows 
or fissures develop. Associated with these local lesions there is 
great anemia, often diarrhea with frothy stools and much loss of 
flesh. When fissures heal, the patches become pallid, and recovery 
takes place. 

The various ulcerated surfaces so far described might be con- 
fused with ulcerative stomatitis, but their chronic character and 
insensitiveness as compared to acute ulcers of the tongue, asso- 
ciated with a specific history or manifestations of tuberculosis or 
syphilis elsewhere, render the diagnosis clear. 

An ulcer on the frenum may be due to whooping-cough, in which 
disease the edge of the lower incisors may injure the tongue in the 
paroxysm of cough, or, in adults, it may indicate the presence of a 
ragged tooth, which produces constant irritation, or, if the patient 
is advanced in years, represent the early stages of epithelioma, or 
that a broken pipe-stem has produced a wound. 

Very rarely the tongue partakes of the ulceration of the tonsils 
and roof of the mouth which is seen in cases of Schonleiirs disease. 



I98 THE TONGUE, MOUTH, PHARYNX, AND CESOPHAGUS 

accompanied by purpuric eruptions on the skin and evidences of 
septicemia. 

Should the tongue be marked by bites from the teeth the patient 
may be an epileptic. Even if he denies that he is affected by the 
disease, the attacks may be unknown to him, because they are 
nocturnal. If the tongue is frequently bitten, the patient may be 
suffering from the early stages of glossolabiopharyngeal paralysis. 1 

The surface of the tongue may be attacked by various eruptions, 
such as measles, variola, eczema, herpes, erysipelas, pemphigus, 
zoster, or hydroa, and from the rupture of the vesicles or bullae so 
formed ulcers may arise. 

If the sore is herpetic, de Mussy asserts that the eruption will 
be found in the distribution of the lingual branch of the chorda 
tympani along the under border at the side. 

Sometimes the surface of the tongue is here and there devoid of 
epithelium, and in some of these patches excoriated. Pain may or 
may not be present. The condition is called chronic superficial 
glossitis by Hack, and is considered by some to be the same disease 
described by Kaposi as glossodynia exfoliativa. It is more common 
in men than women and lasts many years. 

Urticaria of the tongue has been reported by Laveran and xero- 
derma pigmentosum by Keating. 

The presence of a plaque on the anterior portion of the dorsum 
of the tongue to one side of the median line, which is raised, not 
ulcerated, but red and irritated looking, may be due to excessive 
smoking, the smoke irritating the local epithelium. It is always 
very smooth, later covered by a yellowish-brown coat, and is some- 
times called "smoker's patch." It may extend over the whole 
tongue and last for years. 

When the tongue has on its dorsum and edges dull-white or slate- 
colored dots, patches, or lines, which are elevated, hard, and horny 
to the touch, but not painful, the condition is known as leucokera- 
tosis buccalis, or leukoma or ichthyosis, and this may arise from 
smoking or glass-blowing. It rarely begins in persons under twenty 
or in those over sixty years. It is often a strong predisposing agent 
toward cancer of the tongue. These spots are arranged on the 
tongue in longitudinal lines. Hyde asserts that they are due to 
excessive keratinization of the epithelium covered by an adherent 
and dense pellicle. The history is chronic, and ultimately by the 
stiffness of the spots the tongue may become cracked, and this in 
turn, perhaps, gives rise to carcinoma. 

When the tongue is covered by smooth, dense plaques and disks 
or rings, the condition may be lichen planus, but the diagnosis of 

1 It may be pointed out in passing that if there be fits, and biting of the tongue 
never occurs, and the patient is a female, the attacks are probably hysterical. 



THE TONGUE 1 99 

lichen planus from leucokeratosis buccalis is difficult, if not im- 
possible. The plaques are most commonly seen in males between 
twenty and forty years. Closely allied to this is the rare con- 
dition of hardening of the tongue due to scleroderma, as described 
by Kaposi. 

A very rare condition of the tongue is one in which its surface is 
marked by rings or areas on the dorsum, which gradually enlarge 
until they reach the edge or coalesce. In appearance they are red 
and smooth, deprived of filiform papillae, but not of the fungiform 
variety. Often the border of the circle is more red than the centre, 
and the very edge is often yellowish. This condition is sometimes 
called wandering rash, geographical tongue, or annulus migrans. 
Little if anything is known of its cause, save that delicate children 
are most often affected by it. 

Feeble, sickly children sometimes develop upon the tongue, as 
well as on the lips and cheeks, a condition in which a tenacious 
exudation is thrown out, the mucous membrane becoming fissures 
and sore. Gaston and Sebestre have called this stomatitis impeti- 
ginosa. 

Edema of the tongue, with the development upon it of vesicles, 
and, finally, sloughs, may occur, and is probably identical with the 
foot-and-mouth disease of domestic animals. 

Bilateral atrophy of the tongue is due to disease affecting the 
hypoglossal nerves in some part of their course in or below the 
nuclei. (See Paralysis of the Tongue) . It occurs as a symptom of 
glossolabiopharyngeal paralysis, in which case the tongue is shriv- 
elled and atrophied in patches, and in the later stages of the disease 
the organ has a crenated appearance. In other cases it is present 
in progressive muscular atrophy, and rarely in locomotor ataxia. 
It has also been seen in general paralysis of the insane. Unilateral 
atrophy may also occur from these causes, and Remak asserts that 
it sometimes arises from chronic lead poisoning. Any disease 
involving the hypoglossal nerves may so result. (See Paralysis of 
the Tongue.) 

Smooth atrophy of the base of the tongue when developed in a 
person under fifty years of age is a sign of syphilis. Virchow pointed 
out this fact, and it has been confirmed by others. 

In cases where the tongue is much enlarged the increase in size 
may be due to malignant growth, to macroglossia, which is a form 
of congenital lymphangioma, inflammatory hypertrophy, and syph- 
ilis, or acute inflammation from irritant poisons or foods. It may 
also be due to dermoid cysts, fibroma, lipoma, papilloma, angioma, 
myxoma, osteoma, and enchondroma. When it is due to acute 
glossitis the organ is seen to be several times its normal size, is pro- 
truded from the mouth, and marked by the pressure of the teeth. 
The organ is also clumsy and stiff, and heavily coated on the back 



200 THE TONGUE, MOUTH, PHARYNX, AND CESOPHAGUS 

portion. There is a profuse flow of saliva, and swallowing and 
speech are almost impossible. Glossitis may also be due to mercu- 
rialism, to septic infection, and may be either unilateral or bilateral. 
The tongue may be greatly enlarged by actinomycosis. Great 
enlargement of the tongue may also arise in acromegaly and in 
myxedema. In the latter disease the organ is broad, flat, and soft. 

The Movements of the Tongue. — The movements of the tongue 
depend upon its innervation and its muscles, and afford valuable 
information in diagnosis. The rapidity of its protrusion in nervous 
and excitable persons when they are asked to show the tongue is 
noteworthy, and its constant rolling is often seen in persons who are 
feeble-minded. In all diseases associated with mental hebetude its 
protrusion on request is very slow, although the patient will often 
do this act when all other orders to move parts of the body fail to 
produce a response. In the various forms of coma due to apoplexy, 
diabetes, uremia, and cerebral congestion this condition obtains, 
and it is very characteristic of typhoid fever. Often the tongue 
which has been partially protruded is left so, even when the patient 
is told to draw it in. When the patient finds it difficult or impossible 
to remove food from between the teeth and cheek by means of his 
tongue, and complains that the power of speech is interfered with 
because the tongue is clumsy in its movements, he may be suffering 
from the disease known as glossolabiopharyngeal paralysis or pro- 
gressive bulbar paralysis. These lingual disorders are often the 
earliest signs of the disease. More rarely this disability of the 
tongue may arise from pseudobulbar paralysis, or what has been 
called glossolabiopharyngeal cerebral paralysis, a disease in which 
foci of softening occur in that portion of the cortico-muscular tract 
in which are the fibres which supply the muscles used in swallowing 
and speaking. This false type is separated from the true bulbar 
palsy by its sudden onset, an apoplectiform seizure, and other 
evidences of cortical disease. The tongue affords the most im- 
portant points for differential diagnosis when a differential diagnosis 
is to be made under these circumstances, for in the false disease it 
does not waste or develop the reactions of degeneration, whereas 
in true bulbar paralysis these changes always speedily develop. 

Paralysis of the Tongue. — In apoplexy the tongue is protruded 
toward the paralyzed side, as it is also in the condition, already 
described, of hemiatrophy. The lesions of the hypoglossus which 
produce paralysis may be of cortical origin (unilateral), in which 
case the hemorrhage or other injury may be situated where the 
middle and inferior frontal convolutions form the anterior central 
convolution, 1 or in the supranuclear tract between the cortex and 

1 This is probably a fact, but not yet confirmed by autopsy, unless we consider 
Edinger's case of softening under this area, which affected the tongue only, as a 
typical one. 



THE TONGUE 201 

the medulla, or in the hypoglossal nucleus, or, again, in the infra- 
nuclear tract within the medulla. Insular sclerosis may very rap- 
idly cause lingual paralysis. Paralysis of the tongue may also 
result from injury to the hypoglossal fibres outside the medulla 
through meningitis or syphilids or other growths. In still other 
cases pressure upon the nerve in its foramen may cause unilateral 
paralysis, or wounds of the neck, caries of the first cervical verte- 
brae, or cervical tumors may so result. Often in such a case the 
spinal accessory nerve is also involved. Very rarely, indeed, the 
tongue may be paralyzed by a hypoglossal neuritis (Erb) . In rare 
instances hemiatrophy of the tongue is associated with hemiatrophy 
of the face without hypoglossal injury (Gowers). Girard asserts 
that the sensory part of the trifacial contains trophic filaments for 
the tongue, and that the unilateral wasting may be due to disease 
of this nerve. 

It should not be forgotten that paralysis of the tongue may occur 
as the result of diphtheria. 

Hirt asserts that the reaction of degeneration may be found 
in the tongue whether the lesion be cortical or in the nucleus. If 
the lesion is only cerebral, this reaction will probably appear very 
late. 

In paralysis of the facial nerve the tongue may be partially 
paralyzed through the fact that the lingualis muscle is supplied 
by means of the chorda tympani nerve. 

When a tongue which is paralyzed unilaterally is retained in 
the mouth, it is seen that its root on the paralyzed side is higher 
than the other, owing to the paralysis of the posterior fibers of 
the hypoglossus. When it is protruded the tongue goes toward 
the paralyzed side because it is pushed out by the fibres of the 
genioglossus muscle on the well side. 

Finally, if the tongue is paralyzed on one side the lesion is in 
the cortex or the pons on the opposite side of the body, or in the 
nucleus in the medulla on the same side of the body, or in the nerve 
after it has left the medulla. If it is bilateral paralysis the lesion 
is probably nuclear, because the nuclei are so closely situated that 
even a small lesion involves both of them, or it may be due to 
symmetrical disease of both sides of the cortex, the so-called 
pseudobulbar paralysis already spoken of. 

Tremor of the Tongue. — A tremor seen in the tongue may indicate 
a variety of nervous ailments or severe acute disease, as in typhoid 
and other severe infectious diseases, but the freedon from excessive 
coating and the absence of the ordinary signs of acute illness will 
separate the case of tongue tremor of acute disease from the tremor 
representing nervous ailments. 

An important point to be regarded in noting lingual tremor is 
whether the tremor or fibrillary movement is constant, or whether 



202 THE TONGUE, MOUTH, PHARYNX, AND CESOPHAGUS 

it appears only when the tongue is moved to and fro or protruded. 
In typhoid fever the tremor occurs on movement, whereas in glosso- 
labiopharyngeal paralysis when the mouth is open fibrillary move- 
ments of the organ are often marked, while the organ lies in the 
floor of the mouth powerless and beyond the control of the patient. 
Tremor of the tongue is also seen in a marked form in many cases 
of alcoholism and associated with this tremor it will be noted that 
the protrusion of the organ is uncertain or in jerks. 

Spasm of the Tongue. — Spasm of the tongue may be unilateral or 
bilateral, most commonly the latter. It is seen very commonly in 
cases of chorea, particularly of the posthemiplegic type, and in 
hysteria. In the first disease the movements are characteristically 
choreic In the latter the spasm may be tonic or clonic or alter- 
nately tetanic and irregular. 

Often the spasm in hysteria is unilateral. Sometimes it is clonic 
in puerperal melancholia. Spasm of the tongue is a common 
symptom in association with the twitching of the lips of general 
paralysis of the jnsane. Jerky movements of the tongue may also 
occur in insular sclerosis, but this is not the cause of the peculiar 
speech of that affection. 

Very rarely the condition of lingual spasm is due to irritation of 
the hypoglossus by some cause as yet unknown. The tongue is 
darted in or out or thrown from side to side and often injured by 
the teeth. The spasms, as a rule, are not constant, but come on 
in attacks which closely resemble epilepsy, in that they are pre- 
ceded by an aura (Remak and Berger). A very rare affection 
termed aphthongia (Fleury) is characterized by spasm of the tongue 
on attempting to speak. Romberg has recorded a case of lingual 
spasm due to irritation of the fifth nerve from lingual neuralgia. 

In that very rare condition called "Thomsen's disease," " charac- 
terized by tonic spasms in the muscles during voluntary move- 
ments," the tongue may be involved, but in this case the other 
voluntary muscles will share in the affection. 

THE TONSILS, SOFT PALATE, TEETH, AND PHARYNX. 

Having considered the diagnostic significance of changes in the 
appearance of the tongue in this chapter, and of the appearance of 
the lips in the chapter on the Face and Head, there is yet to be 
discussed the condition of the buccal mucous membrane, the tonsils, 
the soft palate, the teeth, the upper part of the pharynx, and the 
postnasal spaces. 

The Teeth. — We can sometimes gain some information from the 
teeth as to the state of the patient. Normally the two lower central 
incisors are cut about the sixth to the eighth month, then the four 
upper incisors from the eighth to the tenth month, and the lower 



THE TONSILS, SOFT PALATE, TEETH, AND PHARYNX 203 

lateral and all the front molars from the twelfth to the fourteenth 
month. The canines are cut from the eighteenth to the twentieth 
month, and the posterior molars at two to two and one-half years. 
The first permanent teeth usually begin to come in about the sixth 
year. In 'children who are sufferers from rickets the teeth decay 
very early and rapidly, but if they be sufferers from inherited 
syphilis, the teeth are often cut in the early months of life.. 

Caries of the teeth to an undue extent is also seen in many 
pregnant women and in cases of diabetes nielli tus. 

If the permanent upper incisors are notched or peg-shaped with 
notches in the free edge, as if cut out with a small gouge, they are 
a fairly sure indication of syphilis of an hereditary character (Hut- 
chinson teeth), and if in association with this deformity of the teeth 
we find middle-ear catarrh and keratitis, we have the " syphilitic 
triad;" which is important as a sign of hereditary syphilis. These 
notches are not found in the so-called "milk teeth." 

The staining of teeth by tobacco or other materials held in the 
mouth may reveal certain habits of the patient, and a blue line on 
the gums where they join the teeth is an indication of the presence 
of chronic lead poisoning. 

Loosening of the teeth, with bleeding, spongy gums should call 
to the physician's mind the possibility of scurvy or scorbutus, and 
the spongy gums are particularly indicative of this affection in 
bottle-fed babies. If loosening of the teeth occurs in adults, it may 
be due to mercurial salivation. 

Grinding of the teeth in sleep in children usually indicates gastro- 
intestinal irritation from indigestion or worms, and it is sometimes 
seen in the advanced stages of respiratory diseases, as from pneu- 
monia or diphtheria associated with dyspnea. It takes place in 
adults in hysteria, maniacal attacks, and in epilepsy. 

The Buccal Mucous Membrane. — Swelling and redness of the 
buccal mucous membrane occur in the various mild forms of 
stomatitis, and in the ulcerative type of this disease the more severe 
lesions are often found in this area. In the malignant ulcerative 
stomatitis called noma the slough which separates from the inside 
of the cheek leaves a large excavation which may become so deep 
as finally to perforate the cheek. 

It is interesting to note that swelling of the cheek with great 
inflammation of the buccal mucous membrane is sometimes seen as 
the result of the formation of a salivary calculus in the duct of 
Steno, and it is also stated that obstruction from inflammation of 
this duct often occurs as a result of poisoning by sulphuric acid. 

This writer has seen a case of that rare malady called Schonlein's 
disease, in which, in addition to the multiple arthritis, purpuric 
eruption, and great edema, the formation of a large ulcer or slough 
threatened to perforate the cheek, and in healing produced a cicatrix 



204 THE TONGUE, MOUTH, PHARYNX, AND OESOPHAGUS 

which interfered with the patient's ability to open the mouth. 
This patient was an adult. 

The Tonsils and Pharynx. — If a patient presents himself to the 
physician with the statement that he is suffering from general pains 
all over the body, particularly in the small of the back, quite high 
fever it may be, with much sore throat and difficulty in swallowing, 
the trouble in the majority of cases will be, in the adults, tonsillitis 
of the follicular form. If the symptoms are exceedingly severe, the 
inflammation may result in suppuration— suppurative tonsillitis. It 
is to be remembered in all cases that the systemic or constitutional 
disturbance is out of all proportion to the severity of the local 
lesions. If it is tonsillitis, the glands can be felt in the majority of 
cases a little beneath and forward of the angle of the jaw, and 
pressure upon them may produce considerable pain. If the mouth 
is well opened and the tongue depressed, there will be found on 
each side of the throat a more or less projecting and inflamed mass, 
in the depressions or follicular openings of which will be found a 
white or yellowish exudate, which in severe cases may spread over 
the surface of the gland until it slightly resembles the membrane 
of diphtheria. Pressure on the tonsil may cause the further pro- 
jection of these cheesy-looking masses. 

In the suppurative form of the disease the surface of the gland 
may be smooth and reddened, and in a day or two become soft and 
fluctuating, and if lanced pus will escape. 

The severe constitutional disturbance, the soreness of the throat, 
difficulty in swallowing, and the follicular exudate call to mind in 
all such cases the possibility of the disease being diphtheria; but in 
tonsillitis the exudate can be easily removed without leaving a 
bleeding surface behind it, and it has not the dusky, dirty look of 
diphtheritic membrane. Again, in tonsillitis the exudate is seen on 
the tonsils only, whereas in diphtheria it spreads over the half- 
arches and uvula. The general symptoms may make one suspect 
the onset of scarlet fever, particularly if the patient be a child ; but 
the examination of the throat in scarlet fever shows the intense 
redness of pharyngeal mucous membrane with comparatively 
slight enlargement of the tonsils. The intense redness of the throat 
in scarlatina and the development of the rash on the skin aid in 
making a differential diagnosis. The lymphatic glands of the neck 
may be enlarged in scarlet fever, but are rarely so in tonsillitis. 

When the swelling of the tonsils is chronic the enlargement of 
these bodies may produce mouth breathing, with the peculiar 
facies of that habit (see illustration in chapter on the Face), de- 
ficient thoracic and general systemic development, and a peculiar 
cough, constant in character and worse at night. Often the swollen 
or enlarged glands extending across the pharynx actually touch 
one another. 



THE TONSILS, SOFT PALATE, TEETH, AND PHARYNX 205 

A rare condition somewhat resembling diphtheritic infection of 
the tonsils is Vincent's angina. There is acute inflammation, a 
diphtheroid membrane, and in some cases swelling of the peri- 
tonsillar tissues and of the cervical lymph nodes. Removing the 
false membrane, as in diphtheria, leaves a bleeding surface. In 
feeble children or adults it may cause death. 

Ludwig's angina causes a much more serious state of the tissues 
than Vincent's angina, as a rule, but varies greatly in severity. In 
its severe forms it is characterized by gangrenous inflammation of 
the sublingual and submaxillary tissues with irregular fever and 
profound prostration. The swelling in both of these areas is hard 
and board-like and the jaw is fixed by the bone induration. If free 
drainage is not established early the septic area breaks into the 
mouth and discharges a sanious fluid, putrefactive in character. 
Death may occur in ten to twelve days. 

If the patient complains of dysphagia, and, on examination, the 
pharynx is red and the tonsils are covered with patches which 
speedily spread, as just described, so that by forty-eight or seventy- 
two hours the tonsils, pillars, and soft palate are covered by a gray 
membrane, the case should always be diagnosticated as diphtheria 
and treated as such, unless a bacteriological examination of the 
exudate shows the infection to be due to a streptococcus and not to 
the Klebs-Loeffler bacillus. Even if the patient has not true diph- 
theria, he may be exceedingly ill. Again, it is to be remembered 
that some cases of scarlet fever which in their early stages present 
a membranous pharyngitis or tonsillitis due to the streptococcus 
in the later stages of the disease may have the Klebs-Loeffler 
bacillus as the cause of the local lesion. The differentiation is to 
be made chiefly by bacteriological tests, but it is worthy of note 
that the early formed streptococcic membrane does not spread 
as does the diphtheritic membrane, and does not return so rapidly 
when removed. The two diseases, diphtheria and scarlet fever, 
often exist simultaneously. Rarely the formation of a false mem- 
brane due to streptococcus infection, or still more rarely to the 
diphtheria bacillus, complicates the course of typhoid fever, and 
also occurs as a grave complication of measles. 

Ordinary sore throat or acute pharyngitis is generally accom- 
panied with little systemic disturbance, the local pain and soreness 
being the most characteristic symptoms. Inspection will show 
the pharyngeal wall red and angry looking, and very likely unduly 
dry. 

Care should always be taken, in the case of children particularly, 
that the early sore throat of measles and scarlet fever is not taken 
for simple pharyngitis. Often the rash of measles can be seen on 
the pharyngeal wall some hours before the rash appears on the 
skin. A peculiar eruption also develops on the buccal mucous 



206 THE TONGUE, MOUTH, PHARYNX, AND CESOPHAGUS 

membrane. This eruption consists of small, irregular red spots 
(Koplik's spots) with a bluish-white centre, and should be looked 
for in a good light. (See Plate VII.) Their absence, however, 
does not exclude the presence of measles. 

They are to be distinguished from the reddened mucous membrane 
of scarlet fever, the large, white spots of thrush, and the sore 
mouth of stomatitis. They do not appear in rotheln. 

Pigmentation of the buccal mucous membrane often occurs in 
Addison's disease. 

Difficulty in swallowing may arise from involvement of the 
pharyngeal muscles in diphtheritic paralysis, or from glossolabio- 
pharyngcal paralysis. (See chapter on the Face, and Retro- 
cesophageal Abscess.) Much more commonly it results from ton- 
sillitis or pharyngitis. Not rarely it is due to a stricture of the 
oesophagus, and sometimes to a morbid growth in the walls of this 
tube, or to the pressure of such a growth situated in the surrounding 
tissues. If the difficulty in swallowing is due to diphtheritic par- 
alysis the history will be that there had been recently an attack of 
diphtheria. If due to a lesion of the bulb there will be the symp- 
toms described in the chapter on the Face, as referred to above. The 
presence of an inflammation of the pharynx or the tonsils is easily 
discovered by observation of the back part of the mouth, as is also 
retro-esophageal abscess, which will generally be found associated 
with disease of the cervical vertebrae. 

If these states be excluded the diagnosis now lies between a 
stricture and a growth, and as the growth may be an aneurysm 
the patient's chest should be carefully examined and the other signs 
of aneurysm sought for, for should this be overlooked and an 
esophageal sound passed, the aneurysm, if present, maybe ruptured. 
The x-ray should be used with a dose of bismuth. (See chapter 
on Stomach and Intestines.) This examination may also disclose 
the existence of a mediastinal growth or enlargement of the 
retro-esophageal glands. If these causes be eliminated the actual 
search for stricture may be begun. 

First the physician should listen over the cardiac orifice of the 
stomach while the patient takes a single swallow of water. If the act 
of swallowing is properly performed this single swallow of water will 
be heard to descend to the cardiac orifice, and then pause there for 
six seconds before it falls into the stomach. If there is a stricture 
this fall will be delayed; if there be atony of the cardia it will be 
hastened. An ordinary esophageal bougie may be passed. If a 
point of resistance is discovered that part of the bougie stem 
opposite the upper incisor teeth is marked, and then the instrument 
is withdrawn. In this manner we are enabled to tell the part of 
the esophagus affected. Usually pain will be felt where the bougie 
is arrested; but care must be exercised that spasmodic contraction 



PLATE VII 



Fig. 1 



Fig. 2 





Fig. 3 



Fig. 4 





The Pathognomonic Sign of Measles (Koplik's Spots). 



Fig. 1. — The discrete measles spots on the buccal or labial mucous membrane, showing the isolated 
rose-red spot, with the minute bluish-white centre, on the normally colored mucous membrane. 

Fig. 2. — Shows the partially diffuse eruption on the mucous membrane of the cheeks and lips: patches 
of pale pink interspersed among rose-red patches, the latter showing numerous pale bluish-white spots. 

Fig. 3. — The appearance of the buccal or labial mucous membrane when the measles spots completely 
coalesce and give a diffuse redness, with the myriads of bluish- white specks. The exanthema on the skm 
is at this time generally fully developed. 

Fig. 4. — Aphthous stomatitis apt to be mistaken for measles spots Mucous membrane normal in hue 
Minute yellow points are surrounded by a red area. Always discrete. 



THE TONSILS, SOFT PALATE, TEETH, AND PHARYNX 207 

of the oesophagus is not mistaken for stricture. In the former state, 
gentle and persistent pressure will overcome the obstruction. 
Usually the stricture exists at a point about six inches from the 
teeth; or where the left bronchus crosses the gullet, about eight 
or nine inches from the teeth; or at the cardiac orifice, which is 
seventeen inches from the teeth in the adult. 

If a stricture exists it may be due to a cicatrix the result of an 
old burn, from the ingestion of alkalies or acids, or from an ulcer 
due to another cause. In other cases the lesion is due to syphilis. 

If the obstruction be due to cancer the passage of a bougie may do 
great damage, and, therefore, if any intimation of the existence of 
such a growth is present, great gentleness must be used. It should 
also be remembered that the bougie may be arrested by its passage 
into a diverticulum, or, in other cases, the instrument, by coiling on 
itself, may give a wrong impression as to the site of the obstruction. 
If a diverticulum is present the food which is obtained from it is 
usually alkaline, as it has never entered the stomach, and milk 
derived from a diverticulum, in which it has tarried a short time 
after attempted swallowing, will not be coagulated. 

In doubtful cases it is advisable to have the patient swallow a 
large dose of bismuth in koumys or kefir and then examine the 
oesophagus with the Rontgen rays. 

Finally, the physician should not forget, if his patient be a young 
woman, that there may be hysterical spasm of the oesophagus. 



CHAPTER VIII. 
THE THORAX AND ITS VISCERA. 

The inspection of the normal and abnormal chest — Their topography — Alter- 
ations in the shape of the thorax — The rhythm of the respirations — The 
results of using inspection, palpation, percussion, and auscultation in 
health and disease — The characteristic signs and symptoms of the various 
diseases of the thoracic organs. 

The chief contents of the thoracic cavity consist of vital organs 
which are, unfortunately, only too often subject to disease. A care- 
ful study of the signs associated with the normal functions of these 
parts is, therefore, of importance, as is also that of the symptoms 
indicating pathological changes. While it is true that in many 
instances patients present themselves to the physician with well- 
marked objective and subjective symptoms pointing to abnormal- 
ities in the organs of the chest, it is also a fact that in many others 
none of these signs exist, or they exist in such an indefinite manner 
that the physician's attention is not attracted to them, and as a 
result important thoracic changes from the normal are overlooked 
or made light of. We base our diagnosis of a case on the changes 
which we find in the thorax as to its contour and as to its move- 
ments, on the respiratory and cardiac sounds, and on the other 
physical signs about to be described. 

The measures used in the physical diagnosis of the diseases 
of the thoracic organs are Inspection, Palpation, Mensuration, 
Percussion, and Auscultation. 



INSPECTION. 

Before we proceed to the study by inspection of this portion of 
the body, we must have a clear conception of the appearance of 
the chest in health. 

Inspection of the normal chest when free from clothing will 
reveal the fact that it is conical in form, the broader part of the cone 
being in the upper portion. Above the clavicles there is usually a 
slight depression (the supraclavicular fossa), and below the clavicles, 
which may be somewhat prominent, there is a slight convexity 
which extends as far down as the fourth rib. This convexity varies 
considerably according to the muscular development of the in- 



INSPECTION 



209 



dividual, the formation of the bony portion of the chest wall, and 
the deposit of fat in the subcutaneous tissues of the chest. The 
nipple is by no means as definite a landmark as is sometimes thought, 
as its position, in respect to the ribs under it, varies greatly in 
different individuals; and it is still further altered in its position by 
the presence of much fat under it, or, again, in multiparous women 




Fig. 54. — The regions of the anterior aspect of the chest. The vertical lines 
are called the mammillary lines. The upper squares form the superior thoracic 
and hypogastric areas; the middle square forms the inferior thoracic area, and 
the lower squares the epigastric. 



by the relaxation of the breast. In the average adult male or 
virgin female the nipple is on a level with the fourth rib or fourth 
interspace. The ribs in a well-developed person are not prominent 
in the upper two-thirds of the chest, but in the lower third are more 
readily seen, particularly at the sides, because of their thin covering 
by the muscles, the subcutaneous tissues, and the skin. The 
14 



2IO 



THE THORAX AND ITS VISCERA 



sternum in front and the spine behind are normally in the middle 
line. Over the top of the sternum is a depression called the 
episternal notch. 

The result of lateral examination of the normal chest when 
compared with the front view will show that the anteroposterior 
diameter is less than the lateral diameter. 

The surface of the chest anteriorly, posteriorly, and laterally has 
been arbitrarily divided by imaginary lines into spaces, as shown in 
the accompanying figure (Fig. 54). The lines running from the 




Fig. 55. — Position of heart in relation to ribs and sternum. Note the small 
part of the left ventricle and the large part of the right ventricle next the 
anterior part of the chest. 



middle of the clavicles downward through the nipple are called 
the mammillary lines. The parasternal line, not shown in the 
figure, is a vertical line half-way between the middle of the sternum 
and the mammillary line; and a line running down the side from 
the axilla is called the midaxillary line. These artificial divisions 
enable us to describe the locality of signs and symptoms. 

If we could see through the chest wall, we would find that the 
lungs extend up to the clavicles particularly on full inspiration. 
Immediately back of the inner end of the left clavicle is the begin- 



INSPECTION 



211 



ning of the innominate vein, and back of this, again, the common 
carotid artery. On the right side the innominate artery bifurcates 
just behind the junction of the sternum and clavicle. The figure 
above shows the relation of the cavities of the heart and its great 
vessels to the chest wall (Fig. 55). 

Anteriorly the lung extends downward as far as the sixth rib on 
the right, but the dome of the liver reaches to the level of the 
fourth interspace. On the left side the lung extends a little lower 
than on the right side. Laterally the lung on both sides extends to 
the ninth rib in the midaxillary line. Posteriorly on the right side 
the lung extends as low as the tenth rib, and on the left side as low 
as the ninth. 





Fig. 5 6. -^The alar chest of phthisis. Fig. 57. — Side view of same patient. 



Marked variations in the shape of the chest occur in healthy 
individuals without possessing any direct pathological significance. 
Thus, it is very common to see one shoulder slightly higher than 
the other, and, in the case of clerks or persons who work much at 
a desk, the left shoulder is very apt to be somewhat elevated. 
Occupations which cause the individual to assume certain posi- 
tions, or to use certain muscles continually, also cause variations 
in the contour of the thorax. 



212 



THE THORAX AND ITS VISCERA 



Inspection of the Abnormal Chest. — The configurations of the chest 
which show a tendency to disease or the results of disease are 
numerous. 

The most familiar of these is the phthisical chest, which has been 
called the "alar chest/' because the scapulae stand out from the 
back like wings (Fig. 56). The anteroposterior diameter, par- 
ticularly in the upper two-thirds, is very slight, and instead of 
convexity of the anterior surface there may be flattening or hollow- 
ness (Fig. 57). This area scarcely moves on inspiration, but the 
lower third, which is bulging, moves markedly with the respi- 
ratory efforts, as does also the epigastrium. The shoulders are very 
sloping; the neck, anteriorly, recedes at the episternal notch, but 
springs forward toward the Adam's apple and the chin. The ribs 
in the phthisical chest fall downward toward the belly from their 
points of origin, instead of coming forward in a normal curve 
(Fig- 57)- 




Fig. 58. — Bulging due to aneurysm of ascending aorta. 



If, on the other hand, the chest bulges anteriorly and posteriorly 
to such an extent that the anteroposterior diameter is greater than, 
or equal to, the lateral diameter, and if this bulging is fairly 
uniform, the shoulders being elevated, the back rounded, and the 
neck short in appearance from the raised shoulders, the patient is 
probably a sufferer from emphysema of the lungs. This chest is 
often called the "barrel-shaped chest" (Fig. 59). The chest wall 



INSPECTION 213 

moves very little or not at all with the respiratory movements, 
which are chiefly diaphragmatic. 

Bulging of one side of the chest wall results, in its most diffused 
type, from the presence of chronic pleural effusion and pneumothorax; 
bulging of a limited area also arises from cardiac hypertrophy, par- 
ticularly that occurring in childhood; from aortic aneurysm , causing 
bulging by pressure (Figs. 58 and 59) ; from pericardial effusion; and, 
finally, from mediastinal growths. Marked bulging over the lower 
part of the chest on the right side should cause us to look for some 
hepatic affection as well as to examine for pleural effusion, and, if 
the bulging is low down on the left side, to examine for pleural 
effusion or enlargement of the spleen. 




<?. 





Fig. 59. — Emphysema of the lungs. Fig. 60. — Bulging of the chest wall, 

Shows barrel-shaped chest. with erosion of ribs, from aortic and in- 

nominate aneurysm. 

Bulging or protrusion of the sternum and the cartilaginous por- 
tions of the ribs attached to it is called " pigeon breast," and is 
due either to rickets, or to the presence of some obstruction to respi- 
ration of a more or less chronic character, during the time the chest 
wall was pliable and capable of being moulded. Sometimes on each 
side of the sternum, over the costal cartilages, there is seen a groove 
or depression as the result of rickets. In other cases a depression 
or groove extends from the ensiform cartilage backward on either 
side toward the spine. This is called ''Harrison's groove," and is 



214 



THE THORAX AND ITS VISCERA 




INSPECTION 



215 



developed in children with poor bony development, and perhaps 
as the result of repeated attacks of asthma or other obstructive 
respiratory difficulty. 

When examining the chests of children the physician will often 
notice swellings at the costocartilaginous junctions, which look 
and feel to the touch like large beads under the skin. These 
beaded ribs are indicative of rickets, and are a manifestation of the 
general tendency to epiphyseal enlargement. This beading is 
usually most marked on the lower ribs (Fig. 61.) 



Fig. 62 



Fig. 63 





Figs. 62 and 63. — Showing shrinkage and partial collapse of left side of chest 
and distortion of spinal column due to chronic tuberculous pleurisy in a boy of 
fifteen years. (From the author's wards in the Jefferson Medical College 
Hospital.) 



Shrinkage of the chest in one part may be due to the contraction 
of old pleural adhesions (Figs. 62 and 63). It is sometimes seen 
over the diseased area in fibroid pulmonary tuberculosis, and may 
be due to wasting of the tissue covering the part rather than to 
any retraction. 

Marked enlargement of the mammary gland on the affected side 
is sometimes seen in pulmonary tuberculosis, particularly in males. 

The shape and surface of the chest having been studied, we can 



2l6 THE THORAX AND ITS VISCERA 

go farther and learn much from inspection of its movements in 
respiration: first, from the rapidity of respiration; second, from the 
respiratory rhythm; third, from the character of the breathing; 
and, fourth, from the movements of the ribs. 

The function of breathing and the movements of the chest are 
closely associated. In men the respiratory movements chiefly affect 
the lower ribs and the abdominal walls, owing to the fact that as 
the diaphragm descends it pushes the abdominal contents down- 
ward, so causing abdominal bulging. In women, however, this is 
not so marked, and the breathing is chiefly costal, the upper part 
of the chest moving more than the lower (costal breathing). If 
abdominal breathing is absent in a man and is replaced by breath- 
ing of the costal type, we can be assured that the movements of 
the diaphgram are impaired by the pressure of fluid in the abdomen 
(ascites) ; by peritonitis, causing fixation of the diaphragm, owing 
to pain; by the presence of large growths in the abdomen, or by 
great enlargement of the liver and spleen. Other possible causes are 
dilatation and distension of the colon, a subphrenic abscess, pancre- 
atic disease, or a greatly enlarged cystic kidney, or hydronephrosis. 

If the costal breathing of a woman is absent, there is nearly 
always some pulmonary cause for it, such as faulty development, 
or, if due to disease, its absence arises most commonly from tuber- 
culosis, or old pleural adhesions which bind down the chest wall. 

When counting the respirations the physician should always 
endeavor to do so without letting the patient know what he is doing, 
since it is difficult for many persons not to control their breathing 
when their attention is called to it. Generally the eye can detect 
the frequency of the breathing by simply watching the movement 
of the chest, or the information can be gained by resting the hand 
on the epigastrium or thorax, while the wrist is also held and the 
doctor is apparently taking the pulse. In the newly born child in 
perfect health the respirations are often as high as 44, but in the 
adult male at rest they are usually about 14 to 16 per minute. 
During sleep the number may fall to 8 or 10. The ratio of pulse 
to respiration is usually 4 to 1, but in rare instances in disease 
it may be 1 to 1. In lobar pneumonia it is often 3 to 1. 

Rapid respirations not due to any recent sudden exertion are 
nearly always indicative of respiratory trouble, primary or second- 
ary. If the primary trouble be in the lung, it will probably be 
due to croupous pneumonia, catarrhal pneumonia, severe bronchitis, 
asthma, tuberculosis, pulmonary abscess, or tumors of the lungs. 
If it be due to secondary lesions in the lung, it may rise from pul- 
monary edema due to nephritis, from congestion or hypostatic 
exudation as the result of a weak heart, from pulmonary embolism, 
from a pleural effusion which seriously interferes with the action of 
the lung or lungs, from growths in the mediastinum pressing upon 



INSPECTION 517 

bloodvessels and so causing exudation into the lungs or pleura, and 
from ascites or abdominal growths pressing upon the diaphragm. 
Usually in these states the respirations will be not only more rapid 
than normal, but difficult or labored. Sometimes in hysterical, 
rapid breathing the respirations reach 150 per minute. This is 
not voluntary, and the diaphragm moves very little, the chief 
breathing being costal. 

If the lungs be clear of trouble, then the difficulty may be 
present in the trachea or larynx, either as the result of spasmodic 
contraction of these passages or because they are occluded by 
growths, such as papilloma or malignant growth, inside or outside, 
or aneurysm which may act by pressure, thereby narrowing the 
tube. Any agency which interferes with the proper oxygenation 
of the blood causes rapid breathing unless at the same time the 
respiratory centre is depressed. 

There are, moreover, several other causes which affect the char- 
acter of the respiration without affecting the larynx or lung tissues 
directly or indirectly. These are fever, which acts as a respir- 
atory stimulant, and excitement, nervous or mental, particularly 
that of hysterical patients. Again, apoplectic seizures, uremia, 
and diabetic coma may be accompanied by rapid breathing. 

The respirations are slowed or decreased in number by great 
obstruction to the entrance of air into the lungs from any cause, so 
that it is difficult to inhale the air, by the action of poisons made 
in the body, as the poisons of uremia and diabetes; by the effect 
of poisons swallowed or absorbed in other ways, notably opium, 
chloral, aconite, chloroform, or antimony. 

The rhythm or relative time of inspiration, expiration, and the 
pause is in health in the mouth and trachea as follows: If 10 repre- 
sents a complete respiratory cycle, inspiration is represented by 5, 
expiration by 4, and the pause by 1. If it is difficult for air to 
enter the chest, as in spasmodic croup, the inspiration is much 
prolonged. This prolongation is also sometimes very marked in 
cases of paralysis of the posterior crico-arytenoid muscles. If 
there is difficulty in expelling the air, the expiration is prolonged, as 
in asthma and in emphysema. 

The most remarkable change in rhythm is the so-called Cheyne- 
Stokes breathing, in which the patient after a pause of several sec- 
onds begins to breathe with gradually increasing rapidity and depth, 
and then, after reaching an acme of hurried respirations, gradually 
decreases their rapidity and depth until they fade to nothing, when, 
after a pause, the same process is repeated. This breathing is seen 
commonly in apoplexy, in uremia, in brain tumor, in cerebrospinal 
fever, in meningeal tuberculosis, in some rare cases of cardiac val- 
vular disease, probably as the result of embolism, and in hematuric 
malarial fever. Rarely it occurs in cases of acute febrile disease. 



2l8 THE THORAX AND ITS VISCERA 

as typhoid fever, scarlet fever, pneumonia, whooping cough, and 
puerperal septicemia. It may also be met with in the coma of 
diabetes. Its presence is an exceedingly bad prognostic sign, but 
cases of recovery after its onset have been observed, and Murri has 
reported a case in which Cheyne-Stokes breathing lasted forty days, 
and Sansom one in which it lasted 108 days. If the cause be an 
acute disease, recovery is more common after this symptom than 
if it be due to some chronic process with an acute exacerbation. 

Labored breathing (dyspnea) is seen in all cases in which the 
blood cannot be provided with sufficient oxygen owing to obstruc- 
tion to the entrance of air into the chest, to spasm of the bronchi- 
oles, or to the occluding of the air vesicles by any form of exudate, 
croupous, catarrhal, or serous. These conditions may be primary 
or secondary to disease elsewhere, as in uremia or cardiac disease. 
Inspection of the chest in such a case shows great activity of the 
accessory respiratory muscles, such as the sternomastoid, the 
scaleni, the pectorals, and the abdominal recti. The nostrils are 
dilated and the face is anxious. The posture of the patient is that 
of sitting up in bed. 

Sometimes when the chest is flexible, as is that of a child, the 
inspiration is jerking when there is obstruction to breathing. This 
is due to the fact that the chest is forced into expansion by mus- 
cular effort, and at the same time is subjected to the external 
atmospheric pressure, while the air enters the lung slowly and 
irregularly owing to the obstruction. 

In this connection should be mentioned the "wavy breathing" 
met with most commonly in pneumonia, a condition in which 
inspiration and expiration do not seem to occur regularly or evenly 
all over the chest, one part filling or emptying a moment before the 
other. This usually indicates a grave pulmonary condition. 

It is also necessary to notice the extent of the chest movements. 
These are very limited in the characteristic chest of a person having 
a tendency to tuberculosis, and in the barrel-shaped and rigid chest 
of emphysema of the lungs. Deficient respiratory movement is 
not only a predisposing cause of lung disease, but an important 
diagnostic sign. When one side of the chest moves more than the 
other to a considerable extent, we suspect, in the side which moves 
slightly, a pneumonia, a pleuritis, a pleuritic effusion or adhesion, 
tuberculous consolidation or fibroid lung, provided that the patient 
has not naturally a greater development on one side than the 
other, or has not pursued a trade or occupation causing unilateral 
hypertrophy. 

While inspecting the surface of the chest the physician should 
also note the presence or absence of enlarged or pulsating blood- 
vessels about the base of the neck. The cervical vessels are 
commonly seen to be distended in cases of advanced emphysema 



PLATE VIII 




A frozen section made in a plane lying 5 cm. in a posterolateral direction from 
the nipples and too near the anterior surface to show the large vessels of the chest 
and neck. The patient died of acute left-sided pneumothorax, resulting from 
tuberculosis. The section reveals the collapsed left lung, the air space about it, 
the heart pushed far to the right in its sac, and the anterior border of the right 
lung compressed by the heart. The right lung is also greatly displaced, and the 
air has pushed the diaphragm downward on the left side. (Ponfiek.) 



INSPECTION 219 

of the lungs and in chronic bronchitis. Systolic pulsation of the 
jugular veins indicates tricuspid regurgitation. Again, in cases 
of thoracic aneurysm pressing upon the superior vena cava and 
innominate vein we find spongy venous masses above the clavi- 
cles, and the veins of the trunk and arms may be engaged. Intra- 
thoracic growths produce similar symptoms. 1 Pulsation in the 
cervical vessels is also sometimes seen in cases of severe anemia 
and in cases of aortic dilatation with regurgitation. 

Sometimes when a patient is placed flat on his back with his feet 
pointing straight toward a window (cross-lights being excluded) and 
the chest exposed, the following phenomenon can be observed 
during forced respiration: along both axillae a sort of shadow is seen 
to descend during deep inspiration from about the seventh to about 
the ninth ribs, passing up again during expiration. It is best seen 
in spare, muscular young persons of either sex. The observer 
should stand with his back to the light. It is called Litten's sign. 

This phenomenon is nearly or entirely absent in the following 
conditions: (1) Fluid or air in the pleural cavity. (2) Obliteration 
of the pleural cavity by adhesions. (3) Advanced emphysema of 
the lungs. (4) Pneumonia of the lower lobe. (5) Intrathoracic 
tumors low down in the chest. 

Slight and limited pulsations on the chest elsewhere than over 
the apex beat may be due to many causes. 2 (See Palpation.) 
When they are seen in the second or third interspace on the right 
side they are due as a rule to displacement of the heart, which has 
been drawn to the right by mediastinopericarditis or contraction of 
the right lung and pleura, or to a thoracic aneurysm. If the pulsa- 
tion is lower than this, it is usually due to a dilated right auricle, or 
displacement of the entire heart, as in a left-sided hydro-, pneumo-, 
or pyothorax. (See Plate VIII.) If the pulsation be on the left 
side of the sternum, then it may arise from a displaced apex beat due 
to effusion, or to retraction of the pleura which has become adherent 
to the pericardium, or fibrosis of the lung may be the cause. 

Finally, there may be marked epigastric pulsation. This is due to 
displacement of the heart by left-sided pleural effusion, which pushes 
the heart to the right and downward, to hypertrophy of the right 
ventricle, to pulmonary emphysema, often a cause of enlargement 
of the right side of the heart, and, finally, it may be due to trans- 
mitted pulsation of the abdominal aorta. If the latter is the cause, 
it can usually be determined by deep palpation that the pulsation 
arises from this vessel. Rarely it is due to the transmission of the 

1 See "The Pathology, Clinical History, and Diagnosis of Diseases of the 
Mediastinum," by the author. Fothergillian Prize Essay of Medical Society of 
London for 1888. 

2 These are spoken of here because they can often be seen yet cannot be felt 
with the finger tips. 



226 THE THORAX AND ITS VISCERA 

aortic impulse by a tumor which overlies the artery. If this is the 
case, it will be found that when the patient takes the knee-chest 
posture the pulsation disappears because the growth falls away 
from the bloodvessel. 

If the epigastric pulsation is in the nature of a systolic retraction 
then it is probably due to indurative mediastinopericarditis. 

Sometimes, on inspection of the chest anteriorly, a curious 
retraction of the interspaces near the level of the apex beat is 
noticed to occur with each systole of the heart. This is usually 
indicative of an adherent pericardium, and when on inspection of 
the posterior surface of the chest such retraction is seen at the 
level of the eleventh interspace it is called "Broadbent's sign" of 
adherent pericardium. This movement is supposed to be due to 
the heart pulling on the central tendon and muscular portion of the 
diaphragm. 

(For the further discussion of the significance and position of 
cardiac pulsations and thrills, see Palpation below.) 



PALPATION. 

Palpation of the chest is usually performed by placing the finger 
tips or the whole hand, palm downward, on the chest. This method 
reveals alterations in its contour and in its elasticity. It will also 
reveal the ability of the thoracic viscera and the chest wall to 
transmit vibrations produced by the voice (vocal fremitus) . This 
so-called vocal fremitus depends upon the fact that below the vocal 
bands lies a column of air which reaches to the vesicular portions 
of the lung, and when an individual speaks this column of air is 
put into vibration, and these vibrations are in turn transmitted to 
the chest wall. Of course, a chest wall greatly thickened by fat or 
by highly developed muscles will not transmit these vibrations as 
readily as a thin chest wall; but aside from these causes of varia- 
tions in fremitus in health we have a number of causes in disease 
which greatly modify vocal fremitus. It must be remembered, too, 
that this vibration is more marked in men than in women and chil- 
dren, because the voice of a man is so much more vibrant and has 
greater volume. Vocal fremitus is also greater on the right side 
than on the left, because the principal bronchus supplying this 
lung is larger than that of the left side, is joined to the trachea at a 
less acute angle, and is nearer the vertebral column; and, again, as 
emphasized by Cary, the bronchus going to the right upper lobe 
is given off at a point very near the origin of the right bronchus, 
and in many cases "fully two and a half inches above the corres- 
ponding left bronchial tube." Sometimes this upper tube comes 
off the trachea directly. (For another theory see page 241.) 



PALPATION 



221 



Palpation of the Abnormal Chest. — The conditions of the lung 
which cause a decrease in vocal fremitus are pleural effusions 
of any kind, which not only cut off the transmission of sound, 
but by their contact prevent vibration of the chest wall; pneu- 
mothorax, which causes collapse of the transmitting medium, the 
lung; any condition which causes occlusion of a large bronchus, 
such as a tumor or a large mass of mucus, and great pleural thick- 
ening. When the vocal fremitus is increased it is an indication of 
pneumonia, of tuberculous thickening or consolidation of the lung, 
of the presence of a cavity or of tumor in the thorax touching the 
chest wall. Fremitus is increased in these conditions because the 
consolidated lung transmits the vibrations of the air in the bronchial 
tubes to the chest wall, or, in the case of a cavity, the sound is 
transmitted directly to it, and it there causes so great a vibration 
of the air in the hollow space that the vibration of the chest wall 
is marked. (In this connection, see part of this chapter on 
Auscultation.) 




Fig. 64. — Area of normal apex beat. 



Palpation of the chest wall will also give information as to the 
position and character of the cardiac pulsations. Thus, the apex 
beat of the heart in persons standing erect will usually be felt, in 
those who are not inordinately fat and who are healthy, between 
the fifth and sixth ribs, about two inches to the left of the sternum 
(Fig. 64). If the apex beat is below this level, its depression may be 
due to enlargement of the heart (hypertrophy or dilatation), to 



22 2 THE THORAX AND ITS VISCERA 

effusion in the pleural cavity on the left side, to pulmonary emphy- 
sema causing abnormal descent of the lung and diaphragm, and 
with it cardiac hypertrophy. Sometimes tumors in the chest 
produce a similar depression of the apex beat. On the other hand, 
if the apex beat of the heart is felt above the fifth interspace, the 
heart may be raised by pericardial effusion or adhesions due to 
inflammation, by pleural adhesions or effusions, by abdominal 
effusion (ascites), by tumors, by distention of the colon with gas, 
and by great enlargement of the spleen. Displacement of the apex 
beat to the left is generally associated with downward displace- 
ment, and is commonly due to hypertrophy of the left ventricle, 




Fig. 65. — Case of large empyema of left side. The x mark near the right 
nipple indicates the displacement of the apex of the heart to the right. The x 
mark in the middle line indicates the apex of the heart after the pus had been 
evacuated. (From a patient in the author's wards.) 



to pleural adhesions, and particularly to pleural effusion on the 
right side. Displacement to the right is due to adhesions and to 
hypertrophy and dilatation of the right ventricle, so that the apex 
beat is felt in the epigastrium or against the edge of the sternum. 
Pleural effusion or pneumothorax on the left side may also cause 
this displacement even as far as the right nipple (Fig. 65). (See 
also Plate VIII.) 

The area of the normal apex beat is about one square inch. In 
disease this area often extends over several square inches, generally 
as the result of hypertrophy and dilatation of the ventricles. 

The force of the apex beat in health depends largely upon the 
depth of the chest and the thickness of its wall. It is increased in 



PERCUSSION 223 

hypertrophy of the heart, when the heart is fully under the influence 
of stimulants, as, for example, digitalis in full doses, in the early 
stages of acute fevers, and in great nervous excitement. If hyper- 
trophy is the cause, the apex beat is usually lower, and more to 
the left than normal, and the impulse is more or less diffuse and 
powerful. 

The apex beat is decreased in force in cases of dilatation of 
the heart without compensatory hypertrophy, in degeneration of the 
myocardium, in cases of effusion into the pericardium and in the 
presence of pulmonary emphysema, which causes the projection of 
a part of the enlarged lung between the heart and the chest wall. 

Thrills felt in the chest wall over the heart may be due to abnor- 
malities in the blood current when valvular disease or aneurysm is 
present. Thus we find thrills in the precordium, or in the neigh- 
borhood of the apex, in disease of the mitral valve, both regurgitant 
and obstructive, but they are usually much more marked in stenosis 
than in regurgitation, which latter condition does not cause much 
palpable thrill, as a rule, except in children. A well-marked thrill 
at the apex is usually to be considered a sign of mitral stenosis if 
it is presystolic in time. Sometimes it extends over the greater 
part of diastole. It is then the so-called " diastolic thrill of mitral 
stenosis," and if a systolic shock or impulse is felt immediately 
after it the presence of mitral stenosis is largely confirmed. Thrills 
in the neighborhood of the second right costal cartilage indicate 
an aortic lesion, generally that of aortic stenosis, of aortitis, or 
of aortic aneurysm. When thrills are felt in the tricuspid area, 
namely, in the midsternal region, or a little to the right of it, the 
lesion is probably tricuspid regurgitation. Tricuspid obstruction 
is very rare. Sometimes a thrill in this area is due to aneurysm 
of the ascending part of the aorta. (See Mitral Stenosis.) 

Pulsation is felt in the chest wall in some cases of empyema. In 
nearly every instance this pulsation, when it occurs, is found on the 
left side. It is produced by the impulse of the heart against the 
effusion, and occurs in two forms: the internal, in which the effusion 
transmits a heaving impulse to the chest; and the external, in which 
there is a pulsating tumor external to the chest wall. Sometimes 
this is called " pulsating empyema." 



PERCUSSION. 

Percussion of the chest is commonly performed by placing one 
finger, generally the middle one of the left hand, on the chest wall 
and tapping it on the back with the tip of the bent finger of the 
right hand, the movement of the striking hand being entirely a 
wrist movement. Sometimes percussion is made by directly striking 



2 24 THE THORAX AND ITS VISCERA 

the chest with the fingers or palm of the hand (direct percussion). 
Some physicians also employ a percussion hammer with a rubber 
head and a pleximeter, or chest piece, of ivory, celluloid, or glass. 
Glass is by far the best material for the chest piece, as it does not 
produce a note of its own when struck by the hammer, as do the 
other materials. The disadvantage of this means of percussion is 
that the physician cannot determine the degree of resistance offered 
by the surface percussed, which is of the greatest service in many 
cases of doubtful character, as, for example, in a case in which 
pneumonia is suspected and the results of the percussion may decide 
the diagnosis. Indeed, more information can be obtained, in 
some cases, by the tactile sense in percussion than by the sound 
which is induced. Care should be taken in performing percussion: 
First, that similar points on the chest wall on each side are carefully 
compared; second, that the finger which is applied to the chest is 
placed in the same relation to the ribs, or interspaces, on each side 
when it is struck; and, finally, in studying the effects of percussion 
the physician should always employ it both during forced inspiration 
and forced expiration, in order to determine the resonance of the 
chest with its full quota of air and when it has only residual air. 

The resonance produced on percussion is due to three things: 
First, to the vibrations of the air in the lungs; second, to the vibra- 
tions of the chest wall when it is struck; third, to the vibrations in 
the pleximeter placed on the chest. The last need be considered 
as a factor only when a piece of celluloid or ivory takes the place 
of the finger, for the finger itself does not vibrate enough to alter 
the note developed. The note produced by vibration of the chest 
wall can also be excluded as of little importance unless the chest is 
very pliable and resilient, as in a thin child, and the blow be deliv- 
ered with force. The most important factor in the production of 
the percussion note is that first named, viz., the vibration of the air 
in the chest caused by the blow delivered on the chest wall. A 
large part of the percussion note depends, therefore, upon the 
amount of air in the chest, the tension of the chest wall, and the 
condition of the pulmonary tissues. The sound produced when 
the healthy chest is percussed is called the normal pulmonary 
resonance. 

In percussion, very different results are obtained by the use of 
light and heavy blows, and when percussing the chest it is wise, 
as a rule, to use light percussion, since a heavy blow may produce 
some resonance in a distant healthy part, and so cause the physician 
to overlook a small localized area of consolidation, which light per- 
cussion might discover. Further than this, it is of great importance 
that the sense of resistance offered to the finger placed on the chest 
in percussion be carefully observed. Many experienced men gain 
more information from this sensation than from the character of 



PERCUSSION 



22 



the note elicited. In consolidation of the lung the elasticity and 
resiliency of the chest are impaired, and in pleural effusion they 
are destroyed. The resiliency and elasticity over cavities are 
marked. The various results produced by heavy and light blows 
are well shown in Fig. 66. 



Light and heavy percussion proO 
duce . pulmonary resonance > 
alone. ' I 



Light percussion develops pul- 
monary resonance. Heavy per- 
cussion reveals dulness due to 
liver under dome of diaphragm. 



Heavy and light percussion gives 
liver flatness. 

Light percussion gives intestinal 
tympany. Heavy percussion re- 
veals li'ver dulness due to its 
lower edge. 



Light and heavy percussion re 
veal gastric or intestinal tynx 
pany. 




Fig. 66. — The effects of heavy and light percussion in outlining organs. 



Percussion of the Respiratory Organs. — On percussing the right side 
of the chest anteriorly in the mammillary line we find in health 
normal pulmonary resonance begins as high as the supra clavicular 
space and extends as low as the fourth interspace or fifth rib, at 
which point the resonance begins to be impaired, so that at the 
sixth interspace or seventh rib we find dulness due to the upper 
border of the liver (Fig. 66). The area of partial and absolute 
hepatic dulness is shown in Fig. 67. 

Posteriorly we find on percussion of the right chest that the 
normal pulmonary resonance begins as high as the suprascapular 
15 



226 



THE THORAX AND ITS VISCERA 



area, and ends as low as the tenth or eleventh ribs. It is much less 
resonant as compared with the percussion notes obtained from the 
anterior aspect of the chest, by reason of the thickness of the chest 
wall and the presence of the scapulas. For this reason pulmonary 
resonance is best developed posteriorly at the bases of the lungs 
below the scapulae. Before percussing the back the patient should 
be made to lean forward and fold the arms, or place his hands on 
his head, in order to stretch the tissues and make them tense and 
as thin as possible. 




Fig. 



67. — Showing area of partial hepatic dulness (outline) and absolute hepatic 
dulness (solid), merging into cardiac dulness in enlargement of liver. 



We can divide the normal sounds produced by percussion into 
the tympanitic, the dull, and the flat. We can also develop by 
percussion of the chest in disease what is known as a " cracked-pot 
sound." 

A tympanitic sound is best produced in its most typical form by 
percussing the epigastrium when the stomach and colon contain 
some gas. When this sound is produced by percussing the chest it 
is due to one of several causes, such as a large cavity, pneumothorax, 
collapse of the lung, or adhesions of the pleural surfaces. A high- 
pitched note on percussion is also a valuable sign in localizing a 
deep-seated consolidation, for while consolidation produces dulness 



PERCUSSION 



227 



on percussion when it is near the chest wall, it is a common thing for 
hyper-resonance to be found in the chest over the area which is 
consolidated if healthy lung supervenes. 

If the cavity be in the lung itself, it must be of some size and be 
near the surface to produce a tympanitic note, and, if it communi- 
cates with a bronchus, the character of the note will change when 
the mouth is closed or opened (Fig. 68). If the case be one of 
hydropneumothorax, changes in the posture of the patient will 
greatly alter the character of the note in a given locality. This is 
also true of many cases of pleural effusion. 



Pectoriloquy. _ 



Consolidated area. 
Fremitus increased. 

Vocal resonance increased. 
Dulness on percussion. 




Increased vocal resonance 
and fremitus. 

Cavity with cavernous 
breathing and gurgling 
rales. 

Hyper-resonance on per- 
cussion. 

Consolidation — bronchial 
breathing. 

Increased fremitus and 

resonance. 
Dulness on percussion. 

Tubercular infiltration. 

Impaired resonance on 
percussion. 

Congestion— crepitant and 
subcrepitant rales. 



Fig. 68. — Tuberculosis at various stages in one lung, the physical signs depend- 
ing on the stage. The upper part is consolidated, and contains a cavity communi- 
cating with a bronchus. 



Consolidation of the lung, as in pneumonia and tuberculosis, 
as just stated, generally gives a dull rather than a tympanitic note; 
but if the consolidated area surrounds a very superficially placed 
bronchus, the percussion stroke may produce vibration in the air 
in this tube, and this will cause a note, high pitched in character, 
which varies as the mouth is closed and opened. (See Fig. 68.) 
Collapse or atelectasis of the lung causes a tympanitic or high- 
pitched note, because the comparatively little air in the lung 
vibrates as a whole, its vibrations not being stopped as in health 
by the tense septa and vesicular walls. This note is best elicited 
in cases of pleural effusion over the apex of the chest, into which the 
collapsed lung has been pushed by the effusion. This is sometimes 
called "Skodaic resonance" and is a very useful diagnostic sign. 
If the compression is sufficient to consolidate the lung, the tympanitic 



228 



THE THORAX AND ITS VISCERA 



note is lost. This note is not altered by opening and closing the 
mouth. 

The " cracked-pot sound" is produced in an adult by the sudden 
expulsion of the air from a cavity through a small opening by the 
force of the percussion stroke. It occurs on percussing a healthy 
child when its mouth is open, the air being forced by the blow from 
the lung through the glottis. It may also be heard in cases of 
pneumothorax with a fistulous tract opening externally or into a 
bronchus, in a few cases of pleural effusion in thin-chested persons, 
and, in rare instances, before consolidation has occurred in 
pneumonia. 




Fig. 69. — Moderate dulness on 
percussion at x over tuberculous 
infiltration. 




Fig. 70. — Showing high-pitched per- 
cussion note anteriorly from consolida- 
tion posteriorly. The shaded area is 
the consolidated part; x indicates the 
position anteriorly where the percussion 
sound is raised in pitch. 



In pleural effusion a flat note is producecl over the effusion, and 
it is of much the same character as the sound elicited by percussion 
of the thigh. (For Grocco's sign see p. 251.) 

Percussion of the Heart and Great Vessels. — On percussing the chest 
anteriorly on the left side at the fourth interspace, it will be found 
that the resonance is decreased by the presence of the heart. 
At the apex of the chest on this side percussion develops normal 
resonance, but as we descend in the line situated half-way between 
the mammary line and the midsternal line we find an impairment 
of resonance at the third rib, which becomes in the next inch of 



PERCUSSION 229 

descent a very marked dulness, produced by the presence of a solid 
organ, the heart. The impairment of resonance is not complete at 
the upper border of the heart, because of the fact that the edge of 
the lung intervenes between the heart and the chest wall, and so the 
note which results on percussion is neither the normal resonance of 
the lung nor the dulness produced by the presence of the heart 
(Fig. 71). The outlines of the normal cardiac dulness on percus- 
sion are shown by the accompanying diagram, and they form what 
have been called the " cardiac triangles" (Fig. 72). 



(Mm 




Fig. 71. — Position of heart partly covered by lungs. The overlapping lung 
modifies cardiac dulness on the left, and in emphysema may completely obscure 
it. (Modified from Aiken.) 

The large triangle begins at the lower edge of the second left 
costal cartilage, and extends down the midsternal line to the level 
of the sixth costal cartilage. The base then extends to the outer 
margin of the apex beat, normally situated in the fifth interspace 
just inside of the midclavicular line. The hypotenuse of the tri- 
angle joins these points. In this area we have included the partial 
and total cardiac dulness. 

The small cardiac triangle, of absolute cardiac dulness, begins at 
the third costal cartilage and extends to the sixth. The base line 
extends to within one and one-half inches of the nipple, and the 
hypothenuse joins this point with the third costal cartilage at the 
midsternal line. (See Fig. 72.) The borders of the heart really 
extend farther than this, but are not near the chest wall and are 
partly covered by lung tissue as already stated. (See Fig. 71.) 



2 3 



THE THORAX AND ITS VISCERA 




Fig. 72. — The cardiac triangles. 




Fig. 73. — Position of heart in relation to ribs and sternum, showing the com- 
paratively small area of cardiac dulness due to the left ventricle. A large part 
of the right ventricle and all of the right auricle are so far back from the chest 
wall as not to produce cardiac dulness to the right of the sternum on percussion. 



PERCUSSION 



23I 



The greater part of the cardiac dulness on percussion is due in 
health to the presence of the right ventricle, which is nearest the 
chest wall. The right auricle also is well forward, while the left 
ventricle only fringes the edge of dulness to the left. This is well 
shown in the accompanying diagram (Fig. 73). 




Fig. 74. — Areas of cardiac and hepatic dulness. 

When hypertrophy or dilatation of the heart occurs, it may be 
found that the area of cardiac dulness extends to the right of the mid- 
sternal line and to the left of the long side of the triangle, and the 
apex beat is apt to be displaced downward and to the left. On the 
other hand inability of the physician to discover any such increase 
in the area of cardiac dulness to the left by no means proves that it 
does not exist, for the enlarged left ventricle often seems to bury 
itself in the left lung even when this organ is normal in size. If the 
lung be emphysematous the difficulty of finding the true left out- 
line is greatly increased, and in emphysema of the lungs the cardiac 
triangles may be obliterated by the extension of the lung between 
the chest wall and heart. They may also be distorted by reason of 
pleural effusions pressing the heart upward and to the right, or in 
the case of right-sided pleural effusion the heart may be pushed 
unduly to the left. Pneumothorax may cause similar results, or, 



232 



THE THORAX AND ITS VISCERA 



again, old pleural adhesions may so displace the lungs or heart 
that the triangles cannot be outlined. (See Plate VIII.) 

Great distortion of the triangles occurs as the result of pericardial 
effusion (see Fig. 75), but in this case the heart sounds will be dis- 
tant on auscultation and the apex beat very feeble or lost, whereas 
in hypertrophy the heart-sounds are exaggerated and the apex 
beat forcible. The diagnosis of pericarditis, after the stage of dry- 
ness and friction sound has passed by, is by no means as easily 
made as some of the text-books would make it appear. One of the 
most reliable signs of pericardial effusion is that of Rotch, namely, 
that any considerable dulness in the fifth right intercostal space 
near the sternum means pericardial effusion, provided right-sided 
pulmonary consolidation and right-sided pleural effusions or adhe- 
sions are excluded. The writer has, however, often seen this sign 
present in marked cardiac dilatation; but if, as Ewart has pointed 
out, there is obliteration of the normal acute angle between the 
right border of the cardiac dulness and the line of liver dulness, this 
sign is of value. (See Fig. 74.) In dilatation of the heart the area 
of the apex beat is usually diffuse, and the heart sounds, while 
feeble, are fairly clearly heard. 

In this connection the following summary, prepared by Sansom, 
of the differential diagnosis between dulness due to pericarditis and 
that due to dilatation of the heart, is of interest: 



Outline of dulness 



Rate of development 
of dulness 



Impulse and apex 
beat .... 



Pericarditis with Effusion Dilatation of the Heart. 

Dulness pear-shaped, and ( Dulness not pear-shaped, 

enlargement chiefly up- \ and enlargement chiefly 
ward. downward. 



Often rapid, and then char- 
acteristic. 

The impulse when present 
is in the third or fourth in- 
terspace; apex beat tilted 
upward and outward, or 
effaced. 



Usually very slow, though 
a rapid dilatation of the 
heart sometimes occurs. 

Impulse can usually be felt 
to the left of the lower end 
of the sternum or in the 
epigastrium. 



Relation of dulness / Dulness may extend to the \ Dulness does not extend to 
to left apex beat . \ left of the apex beat. / the left of the left apex beat 



Often present. 



Pain over precordia 
and tenderness in 
the epigastrium . 

Pulsation in the veins / May be present if endocar- 
of the neck . . \ ditis complicates. 

Usually acute, in course of 
Etiology . \ acute rheumatism, cirrho- 

tic Bight's disease, etc. 

Fever ....<! Often present. 



Usually absent. 

Often present when right 
heart dilated. 

Usually chronic ; often asso- 
ciated with chronic valvu- 
lar lesions, fatty and fibroid 
degeneration. 

Absent unless from some 
complication. 



PERCUSSION 



233 



The same author also tabulates the facts in the differential diag- 
nosis between increased dulness due to pericarditis and that due to 
hypertrophy of the heart as follows : 



Rate of development. 



Impulse, apex beat. 



Pulse 



Pericarditis with effusion. 
Usually rapid. 



Impulse, when present, is 
in the third or fourth 
left interspace, and is 
feeble; apex tilted up- 
ward and outward, or 
beat effaced. 



Weak and quick; may be 
irregular. 



Hypertrophy. 

Usually slow. 

Impulse powerful; if left 
ventricle hypertrophied, 
apex displaced downward 
and outward; if right ven- 
tricle hypertrophied, apex 
displaced downward and 
inward beat may be in 
the epigastrium. 

Character of the pulse de- 
pends on the side of the 
heart which is hypertro- 
phied and the cause of 
left ventricle hypertro- 
phied and no aortic ob- 
struction or mitral regur- 
gitation, the pulse is large 
and powerful. 




Fig. 75. — Outline of percussion dulness in extensive pericardial effusion. The 
light shading is the liver dulness. 



The various valvular and other lesions of the heart result in 
alterations in the size of the various cavities without the entire 




Fig. 76. — Diagram of the area of the heart in aortic regurgitation. The 
dotted lines show enlargement of the left cavities, especially the ventricle, while 
the solid lines show the normal area. 




Fig. 77. — Area of the heart in mitral stenosis. The dotted lines indicate the 
enlargement of the left auricle and enlarged liver. The solid line shows enlarge- 
ment of the right cavities. 



AUSCULTATION 235 

viscus being equally affected. Thus aortic regurgitation causes 
enormous enlargement of the left ventricle (dilatation and hyper- 
trophy), as does aortic stenosis in far less degree (Fig. 76). Mitral 
regurgitation causes hypertrophy and dilatation of the left ventricle 
and some enlargement of the left auricle, and the left auricle is also 
enlarged in mitral stenosis. Tricuspid regurgitation causes hyper- 
trophy and dilatation of the right auricle and hypertrophy of the 
right ventricle, and mitral stenosis often has a similar influence 
over the right side of the heart by damming back the blood into 
the lungs and right side of the heart. The deformities of the 
area of cardiac dulness under these various conditions is shown 
in Fig. 77. 

AUSCULTATION. 

Auscultation of the normal chest reveals in health two sets of 
sounds: the respiratory and the cardiac. 

Auscultation of the Respiratory Apparatus. — The respiratory sounds 
occur in two varieties, namely, vesicular breathing and bronchial 
breathing. The vesicular sound is heard in its most typical form 
over the apices of the lungs anteriorly, the latter at the inferior 
angles of the scapulae posteriorly. We may listen to these sounds 
by placing the ear directly against the chest, or by the use of a 
single or a binaural stethoscope, but neither of these instruments 
is as satisfactory as the ear for this purpose. The patient must be 
in an unconstrained position, as should be that of the physician, 
and if the ear is placed against the chest, or a single stethoscope 
used, the face of the physician should always be turned away from 
that of the patient because the breath of a sick person is often very 
disagreeable and the breath of the doctor may be equally annoying 
to the patient. Care should be taken in the use of the stethoscope 
to see that the edge of the bell in its entire circumference is in close 
contact with the chest wall. 

The respiratory sounds consist, as already stated, in the vesicular 
murmur and the bronchial or blowing sounds, which are sometimes 
designated by the term tubular breathing. In the vesicles the air is 
subdivided into many minute parts, whereas in the bronchial tubes 
it moves along in a column. 

Vesicular breathing signifies a healthy pulmonary parenchyma, 
and when absent one more or less diseased. 

Bronchial breathing, normal in the bronchial tubes, becomes an 
abnormal sign when it is heard in an area in which vesicular breath- 
ing should be present, as will be shown shortly. 

After determining the fact that the sounds of normal vesicular 
breathing are present in the anterior parts of the chest, or that 
those of bronchial breathing can be heard between the shoulders, 



236 THE THORAX AND ITS VISCERA 

we next take note as to the relative duration of the inspiratory and 
expiratory sounds. Normally in the perfectly healthy chest the 
ratio of the inspiratory sound to the expiratory sound is as 3 to 1 . 
In other words, so far as auscultation of the vesicular portion of the 
lung is concerned, inspiration is far longer than expiration. At 
this point we learn one of the most important points in the physical 
examination of the chest, namely, that while the expiratory sound 
may be entirely absent in health, any marked increase in its length 
and loudness, so that it equals or exceeds the inspiratory sound, 
is a sign indicative of some diseased state which impairs the 
elasticity of the lung, such as early tuberculosis, pneumonia, and 
emphysema. 

The other variations in the vesicular respiratory sounds differing 
from those of health are harsh, or, as it is sometimes called, 
puerile breathing and irregular breathing. In children, as the term 
" puerile breathing" indicates, the normal vesicular breathing is 
loud, clear, and harsh, because of the great elasticity of the lung 
and the thinness of the chest wall. If it is exaggerated in a child, 
or present in the areas of normal vesicular breathing in adults, it 
usually indicates some irritation of the bronchial mucous mem- 
brane. If it is found in the apices of the lungs in a marked degree, 
and expiration is prolonged, it is an important and fairly sure sign 
of early pulmonary tuberculosis, or, in acute cases, of catarrhal 
pneumonia or influenzal congestion. 

Sometimes physicians speak of " broncho vesicular breathing," 
meaning a breath sound consisting of both bronchial and vesicular 
sounds. It is sometimes heard in a healthy person when he breathes 
superficially, and in disease usually indicates the early stages of 
pneumonia or early tuberculosis of the lungs. It is of value as a 
diagnostic sign only when localized in one part of the lung. This 
harsh vesicular breathing of exudation and thickening differs from 
normal puerile breathing in this important particular, namely, 
that in the latter expiration holds its normal ratio to inspiration, 
whereas in disease it is greatly prolonged. 

Irregular, "cog-wheel" breathing occurs in the chest of a healthy, 
sobbing child and in that of an hysterical woman, but it possesses 
pathological significance if it occurs when a full breath is taken, and 
it is often present as an early sign of consolidation. 

Bronchial breathing in health is best heard in the posterior part 
of the chest, as already stated, between the scapulae and the seventh 
cervical to the fourth dorsal vertebra. When this bronchial or 
tubular breathing is heard in other parts of the chest it is a sign of 
disease, for while the bronchial tubes are distributed to all parts of 
the lung, the bronchial breath sound is masked by the sounds of 
vesicular breathing and muffled by the lung tissue surrounding the 
tubes. If this vesicular tissue becomes consolidated by disease, the 



AUSCULTATION 



2 37 



vesicular murmur is lost and the solid lung transmits the bronchial 
sounds to the ear of the examiner. Bronchial or tubular breathing, 
or, as it is sometimes called, " blowing breathing," heard in the 
part of the lung in which vesicular breathing is normally heard, 
is, therefore, a sign of pneumonic consolidation (Fig. 78), or of 
compression, or of collapse of the lung above a pleural effusion, or 
atelectasis. Bronchial breathing is also heard in that area of the 
chest in which vesicular sounds normally predominate, in cases 
of cavity of the lung, because in such a lung the bronchial sound 
is transmitted directly to the cavity, and thence to the ear without 
being impaired by the intervention of healthy lung tissue. In 
other words, consolidated tissue and cavities transmit sound better 
than the normal vesicular portion of the lung, which is a combina- 
tion of air and vesicular wall. If the cavity be large, we have a 



Increased vocal resonance and 
fremitus on auscultation and 
palpation. Dulness on percus- 
sion 




Bronchial breathing. | 



Fig. 78. — Pneumonia of the lower lobe with the physical signs of consolidation. 



loud sound developed by the transmission of the bronchial sound 
into its open space and by the passage of air through it. This is 
called " cavernous breathing" If the cavity is not very large, or is 
peculiarly situated in relation to the supplying bronchus, we have 
what is called "amphoric breathing" — that is, a sound like that 
produced by blowing over the mouth of an empty bottle. This 
sound is also rarely heard in cases of pneumothorax in which the 
bronchial tubes, running near to the pleural cavity, transmit their 
sound to the air in the pleural space. 

It is never to be forgotten that in ausculting the chest the two 
sides must be compared, since the well side often gives a standard 
for that affected by disease, and in doing so it must be remembered 
that disease not only modifies the signs in the lung in which the 



238 THE THORAX AND ITS VISCERA 

morbid process is situated, but also changes the normal signs. Thus 
pneumonia or pleurisy or pleural effusion causes a louder vesicular 
and bronchial breathing on the healthy side than is normal, be- 
cause this lung has to take in more air to make up for the loss of 
activity on the diseased side. Great care should, therefore, be 
exercised that the loud, harsh breathing of the healthy part in such 
a condition is not mistaken for the harsh breathing of disease. 

There are a number of other sounds heard in the chest in cases of 
disease of the air passages. These consist in rales of various kinds, 
voice sounds (vocal resonance), friction sounds, and succussion 
notes or sounds. 

Rales are divided into two chief classes, moist and dry. The 
moist are subdivided into the crepitant, or crackling, the fine bub- 
bling, and the coarse bubbling. The dry are called sibilant and 
hissing. Sometimes the sonorous rales are called rhonchi. The 
fine crepitant rale is best imitated by moistening the thumb and 
a finger tip, pressing them tightly together and then separating 
them while they are held near the ear. Another method of 
imitating the fine crepitant rale is to roll the hair where it grows 
above the ear between the thumb and fingers; and still another 
imitation is the crackling of salt when thrown on a fire. This rale 
is due to the separation of the vesicular walls, which have become 
adherent because of exudate. It occurs during the latter part of 
inspiration, and is an important sign of croupous pneumonia in its 
early stages before consolidation has occurred. It also is heard in 
cases of pulmonary collapse and edema, but not always in any of 
these diseased conditions. Care should be taken that the fine rale 
sometimes heard in the chest at the bases, posteriorly, in a person 
who has been long in the dorsal decubitus are not thought to be 
indicative of pneumonia, as they are due only to congestion or 
accumulation of secretion due to posture. 

Fine bubbling rales occur chiefly in the smaller bronchioles and 
the coarse bubbling rales in the larger bronchioles, and they are 
caused by the passage of air through liquid mucus. These rales are 
commonly heard in bronchitis and in pulmonary edema in the lower 
parts of the chest, chiefly posteriorly. If such rales are heard ante- 
riorly or in the areas of vesicular breathing, they indicate the stage 
of resolution of a pneumonia, or if this disease has not been present, 
or is long gone by, they possess the serious import of breaking down 
of tissue from tuberculosis or abscess in the lung. Sometimes these 
rales are limited to inspiration or expiration. In the later stages 
of an attack of asthma they occur with a to-and-fro character, 
and are often musical or tinkling. 

Rales are often removed or altered in character, if not crepitant, 
by coughing. 

It has already been pointed out that dry rales may be divided 



AUSCULTATION 239 

into the coarse and sonorous and the small or fine sibilant rales. 
They are produced by the passage of the air, in the large or smaller 
bronchial tubes, through partly inspissated and sticky mucus. If 
they are sonorous, the larger tubes are the part involved; if sibilant, 
the small bronchioles are affected. 

Metallic tinkling is heard in hydropneumothorax. In this con- 
dition there is a continual dropping of liquid from the apex of the 
chest, or, more correctly, from the compressed lung in the apex 
of the chest, and as the drops fall through the air in the chest 
they strike the surface of the watery effusion with a tinkling sound. 
(See Fig. 80.) 

If a large cavity has formed and liquid is in it, we may hear in 
the chest a peculiar hollow tinkling, called by Laennec " metallic tink- 
ling." These sounds are sometimes heard over the stomach when 
this viscus is in motion and contains a little liquid and air. 

It should not be forgotten that harsh breath sounds made in the 
mouth or in the nose or trachea, may cause the transmission of 
rough sounds or rales into the lungs, which will mislead the phy- 
sician in his diagnosis if he thinks they arise in the pulmonary 
tissues. They can be dissipated or altered in character by clearing 
the throat, coughing, or blowing the nose. 

Friction sounds in the chest depend upon disease of the pleura or 
of the pericardium, generally the former. Normally the visceral 
and parietal layers of the pleurae glide over one another noise- 
lessly, but when they become roughened by disease a sound of 
friction is developed. The friction sound is sometimes so slight 
as to be almost inaudible, and again so harsh as to sound like a 
loud creaking, which not only can be heard, but will convey a sen- 
sation to the hand when it is placed on the chest. As a rule, friction 
sounds due to pleuritis are best heard toward the close of inspiration, 
and occur only in the early stages of the disease, ceasing with the 
development of the effusion and perhaps reappearing as the effusion 
is absorbed. The place where the sound is usually most audible 
is near the axilla. (See Fig. 79.) An indistinct pleural friction 
sound may be emphasized, as pointed out by Abrams, if the patient 
lies on the affected side a few minutes, and then quickly sits up and 
stops breathing. The physician places his ear to the chest wall, 
and directs the patient to take a long breath, when the sound is 
developed. 

If a friction sound is heard at the apex of the chest, tuberculosis 
will often be the cause of its existence. 

Care should be taken that fine rales are not mistaken for friction 
sounds. They can be separated one from the other by the recollec- 
tion of the facts that rales are modified by coughing, are not affected 
by deep pressure on the chest wall, and are usually well diffused, 
while the friction sound is not modified by coughing, is intensified 



2_j.O 



THE THORAX AXD ITS VISCERA 



by pressure on the chest wall, is usually limited to a narrow area, 
and there is often sharp pain. 

An excellent imitation of a friction sound is produced by laying, 
not pressing, one hand over the ear, and then firmly stroking the 
back of this hand by the fingers of the other hand. 




Fig. 79. — Area in which a pleural friction sound is usually heard clearly. 

Vocal resonance is closely allied to the sensation called vocal frem- 
itus, which is felt on palpation, as already described in this chapter. 
It is due to the transmission of the voice sounds down the trachea 
into the bronchial tubes and bronchioles, and thence through the 
various portions of the lungs. If a stethoscope is placed in the epi- 
sternal notch while the patient speaks, and the ear of the examiner 
which is not closed by the instrument is closed by the pressure of 
his finger, the voice of the patient will be very clearly heard. If the 
stethoscope be placed between the vertebral column and the scapula 
posteriorly — in other words, over the bronchial tubes — the voice 
also will be clearly heard, but not as clearly as over the trachea, for 
two reasons : first, because the sound has already been divided into 
the different bronchial tubes, and, second, because the thickness of 
the chest wall muffles it. If the stethoscope be placed over the 
anterior part of the chest toward the sides in the area of typical 
vesicular breathing, the sound of the voice will be still more modi- 
fied, because the sound, like the air that conveys it, is now minutely 
subdivided, and the vibrations are decreased by the multitude of 



AUSCULTATION 24 1 

vesicular walls. Of course, the degree of transmission of vocal 
resonance is governed largely by the character of the voice, and 
for this reason it is more distinct in men than in women. 

If the patient being examined is a man and has a well-developed 
voice, it is usually best to have him speak in a whisper, because the 
full volume of his voice is so great that it will be heard all over the 
chest, and the nice differences between the transmission of the sound 
in the healthy lung and in the diseased area cannot be distinguished. 
Usually we get the patient to speak by asking him to repeat his 
name or count "one, two, three," or by saying "ninety-nine." 
The unemployed ear of the physician should always be closed by 
the tip of his ringer, and the counting or speaking should be con- 
tinued only when the physician has his ear applied to the chest. 

In comparing vocal resonance on each side of the chest in the 
apical region it is to be borne in mind that in almost every normal 
chest vocal resonance and fremitus are more marked at the right 
apex anteriorly than at the left. Fetterolf believes this to be due 
to the fact that the trachea is situated close to the right lung, and 
about 3 centimeters from the left, and does not believe that the 
branching of the right upper bronchus is responsible for the differ- 
ence in the two sides. 

In diseased states of the thoracic viscera we find that vocal reso- 
nance is increased by those changes which aid in the transmission of 
the sound and decreased by those changes which obstruct its trans- 
mission. As pointed out when speaking of vocal fremitus, a solidi- 
fied lung and the opposite state — namely, a cavity — transmit sound 
better than healthy tissue, which is partly air and partly lung tissue. 
We find, therefore, that the vocal resonance, or the sound of the voice, 
of the patient when he speaks, is increased in pneumonia, in tubercu- 
lous consolidation, and in cavity; and is decreased in cases of em- 
physema or in cases in which a pleural effusion separates the lung 
from the chest and deadens sound. Vocal resonance, however, may 
be increased over pleural effusions, particularly the resonance of the 
whispered word. This is called "Baccelli's sign," and Baccelli 
claims that it serves to separate serous effusions from purulent 
effusions, because in his experience it is absent in the latter class 
of cases and present in the former. 1 

When a cavity is situated near the surface of the lung so that the 
sound of the voice is transmitted to it and from it through the chest 
wall with unusual clearness, the sound so clearly heard is called 
"pectoriloquy." It is usually very marked over a cavity connected 
with a bronchial tube. 

Sometimes when the voice sounds through the chest wall as if it 

1 This sign is mentioned here for what it is worth. The writer has never been 
able to use it with success for this purpose. 
16 



242 



THE THORAX AND ITS VISCERA 



were of a bleating character it is called " ego phony." Egophony is 
usually heard at the angle of the scapula, near the margin of a 
pleural effusion, and is supposed to be caused by compression and 
partial occlusion of a bronchus. 

Finally, in pyo- or hydropneumothorax, if the ear be placed 
against the chest and the patient is shaken', we have developed a 
splashing or slopping sound, called " Hippocratic succussion" 
(Fig. 80). It is not always heard in these cases, and may be 
developed when a large cavity in the lung is partly rilled with liquid. 



Compressed 
lung 



Tympany 



Succussion on shaking^ 

Flat on percussion with 
loss of vocal resonance and 
\ loss of vocal fremitus. 




Heart displaced 
Apex beat to the 
right of sternum, 



Fig. 80. — Left pyothorax. Metallic tinkling may be produced by the fluid drop- 
ping from the apex of the chest into fluid below. (After Maydl.) 



THE DIAGNOSIS OF RESPIRATORY AFFECTIONS. 



The healthy physical signs, and their alterations produced by 
diseased conditions of the lungs, have now been discussed. The 
next step is to group these various signs with other characteristic 
symptoms in order that we may obtain a complete picture in the 
diagnosis of a given disease. 

Croupous Pneumonia. — Let us suppose that a patient, previously 
in health or without any serious pulmonary complaint, is found, 
after a physical examination of his chest, to have rapid breathing, a 
somewhat anxious expression, a bright eye, and a dusky flush on one 
or both cheeks. Palpation discovers a hot, fevered skin, which is 
dry or more rarely moist, and increased vocal fremitus over both 
sides of the chest, more marked on one side than the other. Per- 
cussion reveals impairment of resonance over the area where frem- 



THE DIAGNOSIS OF RESPIRATORY AFFECTIONS 243 

itus is found most increased, and auscultation in this area shows 
bronchial breathing, fine crepitant rales, and increased vocal reso- 
nance. Under these circumstances we have before us the physical 
signs of acute croupous pneumonia. The pulse is apt to be rapid (about 
90), but not so fast as the respiration would lead us to suspect, for it 
is a characteristic of this disease that the respirations are out of pro- 
portion to the pulse. The diagnosis is confirmed by the presence of 
pain in the side affected, by the cough, the rusty, sticky sputum, 
and the history that the illness was sudden in onset and was initiated 
by a chill which may or may not have followed exposure. After 
twenty-four hours the rales disappear as consolidation becomes com- 
plete in the affected part, and the area which gave impaired reso- 
nance on percussion now gives a dull note, while the bronchial breath- 
ing in the affected part becomes more marked. The lips are apt to be 
attacked by herpes. With the fall of temperature, or crisis, which 
may be reached by the third to the ninth day, the rales return 
(rales redux) and become more and more loose, coarse, and moist 
as resolution progresses, until the lung becomes entirely clear, 
and only a slight roughening of the breath sounds is to be heard. 
Bad symptoms in such a case are delirium, a feeble pulse, a feeble 
heart with distant heart sounds, or one in which the action is 
labored and irregular. Prune-juice sputa, or, as the disease pro- 
gresses, very purulent sputa, are bad signs also. If the temperature 
falls to normal about the fifth day and then rises again, forming a 
pseudocrisis, the attack will probably be prolonged. 

When a child is affected by croupous pneumonia it is very com- 
mon for us to find all the ordinary objective symptoms without the 
well-developed physical signs just named. The dulness on per- 
cussion is difficult of development unless very light percussion is 
practised, because the chest is so resilient that the percussion blow 
makes the whole chest resound, and it is noteworthy that percus- 
sion of the chest on the diseased side quite commonly develops a 
high-pitched tympanitic note such as we often find above a pleural 
effusion. 

Care should be taken in all suspected cases of croupous pneu- 
monia that another common cause of the same symptoms does not 
mislead the physician. This cause or condition is acute pneumonic 
phthisis. In many cases only the finding of tubercle bacilli in the 
sputum, and the fact that resolution is delayed, and that finally the 
lung breaks down and cavities are formed, will permit a diagnosis 
of acute tuberculosis to be made, although the profuse sweats and 
rapid loss of weight may, before these changes occur, reveal the true 
state. 

There are two areas in the lung often affected very early in 
pneumonia, particularly of the croupous type, and in pulmonary 
tuberculosis, which are apt to be overlooked, namely, the axillse 



244 THE THORAX AND ITS VISCERA 

and the septum between the upper and middle lobe on the right side, 
an area exposed to percussion and auscultation only when the right 
hand of the patient is placed on top of his head in such a way that 
the angle of the scapula is drawn away from the vertebral line (Fig. 
81). If this is done, the inner border of the scapula will approxi- 
mate the line of the septum, and along this line there will often 
be found in this portion of the lung marked dulness on percus- 
sion or, on auscultation, rales and the other physical signs of 




^ 






Fig. 8i. — Area of dulness found in many cases of obscure pulmonary tuber- 
culosis, when the arm is raised so that the scapula no longer covers the septum. 

consolidation, even though the physician is unable to find else- 
where any evidence of local disease to account for the general 
systemic symptoms. Very often careful auscultation of the axillary 
area will also reveal signs not to be found elsewhere, which account 
for the illness, such as those of pneumonia or pleurisy, for here, as 
a rule, the friction sounds of the latter affection are best heard. 

There is another state that gives dulness on percussion, crepitant 
rales, and the other physical signs of pneumonia, namely, pulmonary 
congestion dependent upon the action of a feeble heart in the course 



THE DIAGNOSIS OF RESPIRATORY AFFECTIONS 245 

of prolonged exhausting fevers or mitral disease; but the history of 
the illness, the feeble heart, and the development of these signs in 
the dependent parts of the chest, usually on both sides, effectually 
preclude the idea of any acute inflammatory process in the lung. 

Finally, we frequently have after a pulmonary infarction an area 
of consolidation in the lung; but if this be the case, we also have, 
as a rule, a history of recent hemoptysis and evidences of cardiac 
valvular disease. 

The condition of croupous pneumonia, cannot readily be con- 
fused with any other disease except acute pneumonic phthisis, 
because of its characteristic symptoms, but catarrhal pneumonia 
and tuberculosis of the lung often are confused. 

Catarrhal Pneumonia. — In catarrhal pneumonia the patient usually 
presents a history of recent illness of which the pulmonary state is 
a sequence or the pulmonary complication comes on in the course 
of an acute illness of another kind. The disease rarely begins with 
the marked and startling symptoms of the croupous form, but is 
insidious and accompanied by a milder but more prolonged fever. 
Percussion often will not give the positively dull note which can be 
elicited in croupous pneumonia, and only impairment of resonance 
may be developed. There are increased vocal fremitus on pal- 
pation and increased vocal resonance on auscultation; there are 
also increased bronchial breathing and more bronchial rales than 
in the croupous form, for the disease is a bronchopneumonia in- 
volving the bronchial tubes and adjacent tissues. The signs are 
generally diffuse, very often heard best at the bases posteriorly, 
and clear tubular breathing, such as is heard in the croupous form, 
is rarely to be found. The sputum is not sticky or rusty; the fever 
does not end by crisis, but rather by lysis; and the lung returns to 
its normal state very slowly, its condition sometimes remaining 
almost stationary for weeks at a time. 

The separation of these symptoms of catarrhal pneumonia from 
those of early pulmonary tuberculosis is practically impossible by 
the physical signs until the case has progressed to a well-advanced 
stage. The sputum should be well watched for tubercle bacilli. 

Pulmonary Tuberculosis. — Often catarrhal pneumonia merges into 
tuberculosis, and very often the diagnosis of catarrhal pneumonia 
proves to have been made in a case in which the disease is really 
primarily tuberculosis. 

Indeed, so far as the physical signs are concerned, there is no 
difference between those of influenzal congestion, catarrhal pneu- 
monia and early tuberculosis, since in all of them there is impaired 
resonance on percussion, prolonged expiration, harsh inspiration 
and, sometimes, fine rales. All of these signs indicate only that 
there is a divergence from normal in the part of the lung where 
they occur. In the early stage, before breaking down occurs, it is 



246 THE THORAX AND ITS VISCERA 

vitally important that percussion be carefully practised, since im- 
paired resonance shown by light percussion is often the first devia- 
tion from the normal that can be recognized. The percussion 
should be so lightly performed that the physician obtains as much 
information from the sense of resistance as from the note he pro- 
duces. Care should be taken that the slightly less resonant note 
at the apex of the lung as compared to that at the right is not 
taken for a sign of disease, for such a variation is present in many 
normal chests. 

We have to rest the diagnosis of tuberculosis chiefly on the 
physical signs, the personal history, the fact that recovery does not 
speedily take place, and that the patient loses weight more or less 
rapidly, and the presence, as the case becomes well advanced, of 
tubercle bacilli in the sputum, and, later, of yellow elastic fibres 
which indicate a breaking down of the lung tissues. 

A patient after complaining of a persistent "cold" with more or 
less cough fails to get better, and suffers from loss of appetite, loss 
of weight, and develops chills and fever, also becoming more or less 
anemic. In such cases it is particularly necessary that the physician 
be on the qui vive for the physical signs of pulmonary tuberculosis, 
as this is the stage in which the disease is still curable in many 
instances. In such patients a slight, prolongation of expiration, 
with harsh inspiration, and impairment of resonance on percussion, 
particularly at one or both apices, may be the only, yet very 
important, physical signs. 

If the malady be tuberculosis and progressive, we soon find in 
the chest and sputum signs which make the diagnosis clear. On 
inspection the costal breathing is less than normal; the hand placed 
upon it feels, when the patient speaks, that there is not only in- 
creased fremitus, but a bubbling feeling from coarse rales, and 
auscultation also reveals moist rales, the signs of the breaking down 
of lung tissue (Fig. 82). Finally, when a cavity is developed the 
percussion sound over it becomes high-pitched, and, if the cavity 
be large, almost tympanitic, although all around it dulness may be 
present. If the cavity is large, it will often be found that it is 
possible to develop a still more tympanitic percussion note if at 
the same time that the chest is percussed the patient holds his 
mouth open. This is called "Wintrich's change of note." The 
breath sounds now become more tubular or amphoric, and vocal 
resonance may be increased to such an extent that bronchophony 
or pectoriloquy becomes marked even in that part of the lung in 
which in health the vesicular sounds are heard most typically 
(Fig. 83). Prolongation of expiration is also present, and sweats, 
irregular hectic fever, and great loss of flesh ensue. 

When there is fibroid phthisis of the lungs, inspection of the thorax 
often shows marked retraction of one side of the chest, more often 



THE DIAGNOSIS OF RESPIRATORY AFFECTIONS 



247 



the left side in front near the apex. The supraclavicular fossa and 
the costal interspaces are apt to be retracted, the scapula drawn 




Fig. 82. — Areas of fine moist rales in early stages of tuberculosis of apices of 
lungs with impaired resonance on percussion and prolonged harsh expiration. 




Fig. 83. — Case of pulmonary cavity due to tuberculosis. The central ring- 
is the area giving the physical signs of cavity, with cavernous breathing and 
whispering pectoriloquy, and the outer ring thai of consolidation (dulness), 
with rapid breaking down of the lung tissue (moist rales). 



248 THE THORAX AND ITS VISCERA 

nearer the spine, and that side of the thorax is poorly expanded on 
inspiration. The respiratory murmur is feeble and distant, and 
resonance on percussion is below normal. If secondary pleural con- 
tractions occur, the heart may be drawn from its normal position 
and the other lung is apt to give a high-pitched percussion note. 
This form of pulmonary tuberculosis is usually very slow and 
lasts for years. 

In striking contrast to the form just described is acute pneumonic 
phthisis, already referred to, which often begins with the suddenness 
of an acute croupous pneumonia, with a chill, blood- tinged sputum, 
and pain in the chest. When the consolidated lung fails to undergo 
resolution the sputum is examined and if tubercle bacilli are present 
they reveal its true nature. 

In some cases of suspected pulmonary tuberculosis the Rontgen 
rays can be used with great success in aiding difficult diagnosis. It 
is best to employ the nuoroscope rather than the radiograph, since 
with the former different parts of the chest can be rapidly compared, 
and the focus readily changed for deep and superficial tissues. Con- 
solidated areas are dark and shadowy; cavities are light, surrounded 
by shadow. Nearly always in such cases marked enlargement of 
the bronchial lymph nodes are discernible. So, too, abscess of the 
lung produces a distinct shadow in many cases. 

Finally, it is to be recalled that mitral stenosis or regurgi- 
tation may, by producing engorgement of the lung, produce 
physical signs closely resembling pulmonary tuberculosis, for there 
are continued cough, dyspnea, blood-spitting, and loose rales on 
auscultation. The absence of tubercle bacilli, and the presence of 
large cells filled with brown pigment in the sputum show the cause 
to be cardiac. 

Pulmonary Abscess. — The history of the case and its symptoms 
are our chief means of separating pulmonary abscess from pul- 
monary tuberculosis with the development of cavity, for the phy- 
sical signs are often the same. In cases of abscess we find that the 
patient has suffered from pneumonia or from pyemia with embolic 
infarction. In other cases foreign bodies from the nose and throat 
entering the lungs produce such lesions. The symptoms of abscess, 
which separate it from cavity due to tuberculosis, are as follows: 
in abscess the lesion exists in the lower lobe, as a rule, while the 
tuberculous cavity is usually found at the apex or in the upper lobe. 
The constitutional disturbance in abscess is often very slight, 
whereas in advanced tuberculosis it is usually severe. In abscess 
the sputum is copious and purulent, and often coughed up in 
gushes, whereas in tuberculosis it is often scanty, and not markedly 
purulent, as a rule. Again, in the sputum of the last-named disease 
tubercle bacilli may be found, but they are absent in abscess 
unless tuberculous infection is simultaneously present. 



THE DIAGNOSIS OF RESPIRATORY AFFECTIONS 249 

The use of the fluoroscope is of great value in localizing the pus 
in some cases. 

Pulmonary Gangrene. — If the patient has the signs of cavity of 
the lung, and in addition an exceedingly fetid breath, with great 
wasting, the case is one of pulmonary gangrene. Gangrene is 
usually found at the base of one lung, as is abscess. The sputum 
is usually brownish. 

Bronchiectasis with fetid breath is occasionally met with, but the 
fetor after coughing is never so exceedingly offensive as it is in cases 
of gangrene. 

Pulmonary Edema. — The physical signs of pulmonary edema may 
develop suddenly as a result of an injury to the vagus, or in 
disease of the kidneys, lungs, or heart. The onset is insidious, 
but the rapid breathing, the moist rales, the existence of these 
signs chiefly in the lower part of the chest, the bilateral character 
of the signs combined with dulness on percussion, the absence of 
fever, the frothy sputum, and, it may be, the associated presence 
of renal or cardiac disease, all point to the true state of affairs. 
Such a state not rarely develops in the course of pulmonary 
congestion in old persons, particularly if influenza is the cause. 
It develops most commonly, however, as a complication of 
nephritis. 

Pleuritis. — Let us suppose that a healthy man is seized with pain 
in one side of the thorax and a chill followed by fever. An examina- 
tion of his thorax will reveal on inspection deficient breathing on 
the affected side, which is more or less fixed because of pain produced 
by the inflamed pleural surfaces moving over one another on inspi- 
ration. Exaggerated breathing will be found on the opposite side 
to compensate for this fixation, and auscultation on the painful 
side will reveal a friction sound, probably best heard in the axilla. 
(See Fig. 79.) 

Pleural Effusion. — The signs of pleural effusion are impaired 
mobility, or fixation of the affected side and obliteration of the 
interspaces where the fluid exists. The chest is flat on percussion at 
the most dependent part of the pleural sac, namely, at the base of 
the lung posteriorly and later laterally, and finally this area of 
flatness on percussion gradually rises higher and higher until the 
effusion is completed. It extends anteriorly, and may be demon- 
strated as well here as it can be posteriorly and laterally, although, 
if the patient lies on his back or is partly recumbent, the entire 
anterior surface of the chest may be hyper-resonant, owing to the 
fluid leaving the front of the chest and going to the more dependent 
parts. In other words, in cases of non-sacculated serous pleural 
effusion changes in the position of the patient cause alterations in 
the area of flatness on percussion, unless the effusion is large enough 
to entirely fill the chest, when, of course, it is immovable. Inspection 



250 



THE THORAX AND ITS VISCERA 



will show an increase in the size of the chest on the diseased side, 
with bulging of the intercostal spaces. 

Above the level of the effusion percussion over the compressed 
lung gives a somewhat hollow note or hyper-resonance, called 
"Skodaic resonance," and the sense of resistence to the percussed 
finger is less at this point than over the effusion where the resistance 
is great. Percussion and palpation will reveal the lower margin of 
the liver depressed if the effusion is on the right side (Fig. 84). 




Fig. 84. — Right-sided pleural effusion. The area of flatness on percussion in the 
thorax merges with that of liver dulness, and the lower border of the liver is 
below its normal level. The apex beat is displaced to the left at x. The circle 
represents Traube's semilunar resonant space, which is obliterated in left-sided 
effusion, but not in right-sided effusion. 



Inspection and palpation will show the apex beat of the heart 
displaced to the right and downward in cases of effusion into the 
left pleura, and to the left in cases of right-sided effusion. Again, 
if the effusion be on the left side, it will be found on percussing 
" Traube's semilunar space," a space directly in the mammillary 
line and a little below the nipple that the usual tympanitic 



THE DIAGNOSIS OF RESPIRATORY AFFECTIONS 25 1 

resonance normally found in this area is extinguished through the 
downward pressure of the fluid (Fig. 84) . 

In some cases of pleural effusion careful percussion posteriorly 
at the base of the opposite side of the chest from that of the effu- 
sion, close to the spine, will reveal marked dulness. This area of 
dulness is triangular in shape with the base of the triangle near the 
diaphragm and its apex several inches up the side of the vertebral 
column. This is called Grocco's sign or the "paravertebral triangle 
of dulness of pleural effusion." 

In ausculting the chest in the area in which flatness has been 
developed by percussion the breath sounds are very indistinct, 
except in the back near the vertebral column, where there may be 
marked tubular breathing. If the patient speaks, there will be 
found loss of vocal resonance and of fremitus over the effusion, but 
along the margin of the spine on the diseased side there may be 
heard in some cases bronchophony, or even the bleating voice 
sound called egophony. 

It is a noteworthy fact, however, that the physical signs on aus- 
cultation vary with the method of examination which is employed, 
for if the stethoscope is used the breath sounds are often inaudible, 
whereas, if the unaided ear is used bronchial breathing may be dis- 
tinctly heard. The presence of bronchial breathing over an area 
supposed to contain fluid does not negative this diagnosis if the 
unaided ear is employed. While it seems paradoxical that sounds 
can be heard with the naked ear which are inaudible with an aided 
ear the paradox is explained by the fact that when the stethoscope 
is used only a very limited portion of the thoracic contents is 
ausculted. 

Finally, if the effusion is absorbed by unaided nature, the area 
of flatness on percussion becomes less and less from above down- 
ward, the expansion of the chest on inspiration increases, the inter- 
spaces cease to bulge, and the friction sounds may return for a brief 
period. 

Particular attention should be called to the possibility of pleural 
effusions coming on insidiously. There is probably no other massive 
pathological change anywhere in the body so often unsuspected or 
overlooked, and it is noteworthy that, when pleural effusion is 
insidious in its onset and devoid of prodromes, it is often due to 
an undiscovered tuberculosis, whether the exudate be found to be 
serous or purulent. Again, the fact that tubercle bacilli cannot be 
found in the effusion when it is aspirated in no way proves that 
the effusion is not tuberculous in origin, since they are rarely found 
in the fluid even when tuberculous pleurisy is most active. 

Serous pleural effusion, single or double, may occur as part of the 
dropsical condition in renal or cardiac disease, from disease of the 
blood itself, or it may result from thrombosis of the vena azygos. 



252 THE THORAX AND ITS VISCERA 

The latter cause is particularly apt to come on in patients suffering 
from typhoid fever or other exhausting diseases. 

A right-sided effusion may arise from heart disease which pri- 
marily enlarges the right side of this viscus and presses on the 
pulmonary veins, causing a transudate from the visceral layer of 
the pleura. When a left-sided effusion is due to this course the 
enlargement of the left auricular appendix of the left ventricle 
presses on the pulmonary vein. 

If on aspirating the fluid in the chest it is found to be hemorrhagic 
'in character, the cause may be one of the diseases which produce 
marked asthenia, notably carcinoma, nephritis, one of the acute 
infectious diseases in a malignant form, or tuberculosis. The 
cancer may or may not be in the chest. Rarely such an effusion 
occurs in otherwise healthy men without these causes. The 
possibility of the hemorrhagic effusion being due to a leaking 
aneurysm, or to leakage from an ulcerated bloodvessel in tuber- 
culous disease of the lung is to be remembered. 

Empyema. — If the effusion is purulent, the patient generally loses 
flesh and strength, and he may have chills, fevers, and sweats. 
Particularly is this result prone to follow a pleurisy complicating 
one of the acute infectious diseases, such as scarlet fever, typhoid 
fever, pneumonia, and in cases in which tuberculosis is responsible 
for the illness. In children empyema is not so serious as it is in adults. 
In the former it is often due to the pneumococcus, in the latter to 
the streptococcus. 

Empyema may also be due to the Bacillus typhosus, the colon 
bacillus, the microorgansirn of influenza, the gonococcus, and actino- 
mycosis. 

Sometimes interlobar pleurisy develops and effusion of fluid or of 
pus takes place in such a position that it lies between the two lobes 
without escaping into the general pleural cavity. Under these con- 
ditions the symptoms of an ordinary pleuritis may be present, and 
the physical signs will consist of an area of flatness on percussion, 
which is sharply outlined, and is bordered above and below by an area 
of high-pitched resonance on percussion, and tubular breathing due 
to compression of the lung. 

Hydropneumothorax. — If the effusion be accompanied by pneumo- 
thorax, we will find three sets of physical signs, namely, those of 
effusion, which will be at the lowest part of the chest, next above 
this an area in which percussion gives a clear tympanitic note due 
to the air in the pleural cavity, and above this the physical signs 
of the compressed lung on the apex of the chest cavity. In this 
condition we may hear succussion or splashing sounds, if the 
patient is shaken while sitting up and the physician's ear is against 
the chest wall, and the metallic tinkling, or dropping sounds, as the 
fluid falls from the top of 'the chest cavity into the effusion. (See 



THE DIAGNOSIS OF RESPIRATORY AFFECTIONS 253 

Fig. 80.) Again, we may use what has been called "coin per- 
cussion." This consists in having an assistant place a large silver 
coin against the chest wall on the diseased side anteriorly, and 
then the physician listens at the posterior aspect of the chest, his 
unused ear being closed by his finger. The assistant now strikes 
the silver coin with the edge of another silver coin. If the coins 
be struck together below the surface of the effusion, very little of 
the metallic sound will be transmitted through the chest. If the 
coins are struck together at the level of the layer of air, the 
sounds come through the chest cavity with startling clearness; but 
if at the level of the lung, they are less clearly heard than at the 
level of the air, but more so than at the level of the effusion. 

The reasons for this are obvious, for the liquid prevents transmis- 
sion of the metallic sounds, as does also to some extent the com- 
pressed lung at the apex of the chest, whereas the space filled with 
air conveys the sounds directly to the ear. 

Pneumothorax. — The sudden development of dyspnea and thoracic 
pain, with pallor and cyanosis, a subnormal temperature and a 
rapid pulse, during the course of a case of tuberculosis of the lung 
in particular, should lead us to suspect pneumothorax. Inspection 
shows distention of the affected side, bulging of the intercostal 
spaces, and a sensation to the physician's hand of distention of the 
chest. The act of respiration moves the involved side but slightly, 
while the opposite side is moved greatly. The apex of the heart 
is displaced and percussion gives a loud hollow note. Auscultation 
of the affected side reveals absence of breath sounds, and the 
hyper-resonance on percussion, with absence of respiratory murmur, 
makes a very pathognomonic combination of symptoms. Metallic 
sounds are often elicited in this condition arising from unknown 
causes. It will be found that if the pleximeter is struck with the 
handle of a percussion hammer, while the physician auscults the 
chest elsewhere, a clear distinct metallic sound is transmitted to 
the ear. When a pneumothorax communicates freely with a 
bronchus we often have gurgling or bubbling sounds due to 
bronchial secretion, or if pus is in the thorax, we find moist rales in 
the bronchial tubes and purulent expectoration. It is remarkable 
how differently patients suffer when affected by pneumothorax. 
Some are in the most urgent dyspnea, but others after a very 
short time seem to be able to take some exercise without grave 
embarrassment. 

Bronchitis. — If after exposure to cold there is a sense of soreness 
in the chest, with more or less oppression and a hard cough, which 
seems to wrench the bronchial tubes, the cough not being associ- 
ated with expectoration, and the febrile movement but moderate, 
we suspect the presence of an acute bronchitis; a diagnosis which 
will be confirmed if we find the following physical signs: 



254 THE THORAX AND ITS VISCERA 

There is marked roughening of the breath sounds all over the 
chest, particularly over the bronchial tubes at the back, between 
the scapulae, without any increase in vocal resonance and fremitus 
or any impairment of resonance on percussion. As the disease 
progresses these sounds of harsh breathing give way to rales, which 
are at first fine and moist, then coarse and sonorous, as the second 
stage, or stage of secretion, develops; and, finally, they decrease 
little by little, as health is approached and the mucus is expelled by 
coughing. Care should always be taken to determine in examining 
a case of suspected bronchitis that the symptoms are not due to a 
bronchopneumonia. 

Should the case become chronic, the coarse and more or less 
sonorous rales will persist and become constant. Such cases 
usually become worse in winter, and the sputum is sometimes 
very profuse (bronchorrhea) . 

The physician should always be careful in these cases to see 
to it that renal disease or a feeble heart is not the cause of the 
bronchial disorder. Too often the careless diagnosis of chronic 
bronchitis is made when the trouble is due to pulmonary tuber- 
culosis or a feeble heart. The 
^g^^^ health suffers but little in simple 

jpffl Ik chronic bronchitis ; but if bronchi- 

H ectasis develops it may be much 

^ "Jk impaired. 

^ •'*? Under the name u putrid bron- 

^k chitis" we have a state in which 

%;' : v \ the sputum is foul and expelled 

/ \ in a liquid form, in which float 

I little yellow plugs (Dittrich's 

plugs). This condition may end 
M in pulmonary gangrene or cause 

,*. metastatic abscess. It is practi- 

cally a severe form of bronchi- 
ectasis. 
Emphysema. — The presence of a 
d? , barrel-shaped chest (Fig. 85) with 

/ almost immovable walls and 

marked abdominal breathing, 
points to the presence of emphy- 
sema of the lungs, and this opinion 
is confirmed if on auscultation of 
Fig. 85.— Emphysema of the lungs, the chest we find marked^ pro- 
Shows barrel-shaped chest. longation of expiration, diminished 

vocal resonance and fremitus, 
and increased resonance on percussion. The face is often quite 
cyanotic, the superficial veins of the neck turgescent, the ab- 




THE DIAGNOSIS OF RESPIRATORY AFFECTIONS 255 

dominal respiratory movements abnormally great, and the super- 
ficial veins in the epigastrium enlarged. If bronchitis or bron- 
chiectasis is associated with the emphysema, as is frequently the 
case, we find more or less marked rales all over the chest, par- 
ticularly posteriorly. Sometimes a systolic murmur can be heard 
over the tricuspid area, due to regurgitation in the right side of the 
heart. Cardiac dulness is generally obliterated by the enlarged 
lung, and the apex beat cannot be felt except in the neighborhood 
of the ensiform cartilage or in the epigastrium. Both the hepatic 
and splenic dulness are found to begin and extend lower than 
normal, owing to the expansion of the lung. We may also find 
accentuation of the second sound in the pulmonary artery. Tri- 
cuspid regurgitation not rarely develops as a result of a damming 
up of the blood in the right ventricle. 

Asthma. — When a patient is seized with a violent attack of 
dyspnea its cause may be asthma, a foreign body in the larynx, 
laryngeal spasm, or pulmonary edema. In asthma there is labored 
breathing in which all the accessory muscles of respiration in the 
neck and trunk aid the ordinary respiratory muscles. The posture 
of the patient will usually be that of sitting up in bed and somewhat 
leaning forward. The face will be flushed, the vessels of the face 
and neck turgid, and the lips may be cyanotic. Often the patient, 
while sitting up, supports himself by resting on his hands, which 
are placed at his side in order to raise his shoulders and fix the 
chest walls for contraction of the muscles which are endeavoring 
to drive out the air, for it is to be remembered that the respiratory 
difficulty in asthma depends more upon the fact that the patient 
cannot empty the lungs than upon the fact that he cannot fill 
them. As a matter of fact, they are too full of air which has 
been used. 

Inspection not only shows these signs in asthma, but also reveals, 
in cases in which emphysema has not developed to such an extent 
as to cover the heart with the lung, that the apex beat is diffused 
and the heart laboring. Palpation reveals little except when 
coarse rales are present in large numbers, when some bubbling 
may be felt. 

Percussion usually gives an increased resonance, because the 
chest is inordinately full of air, and auscultation reveals very loud 
blowing breathing, musical notes, or squeaking or creaking noises, 
both on inspiration and expiration. Finally, as secretion begins 
to be established, musical and cooing rales may be heard, in well- 
marked cases, all over the chest before the ear is placed against 
the patient. At first these rales are heard chiefly on expiration, 
but very shortly they occur equally loudly on both inspiration 
and expiration. 

If on auscultating the chest we find it filled with musical and 



256 THE THORAX AND ITS VISCERA 

cooing rales heard in every part, although most marked in the 
bronchial tubes, we may be fairly sure that an attack of asthma is 
about passing away; but if, on the other hand, the attack is begin- 
ning, the manifest difficulty in breathing, the prolonged expiration 
with comparatively few rales, the harsh bronchial sounds, and the 
general objective symptoms of the case will explain the cause of 
the pulmonary condition. (See chapter on Cough and Expector- 
ation.) 

As asthma is a symptom, not a disease in itself, the physician 
should always examine the nose, with the object of discovering 
some source of reflex irritation in the nasal mucous membrane, or 
test the urine to discover whether renal disease is present, or the 
heart to determine if a cardiac lesion accounts for the symptoms. 
Sometimes gastric disorder is responsible for the attack. 

Care should be taken that a catarrhal pneumonia developing 
after an attack of asthma is not overlooked until the patient is 
dangerously ill. 

Foreign Bodies in the Air Passages. — The dyspnea due to a foreign 
body in the air passages, whether it be a piece of meat or a false 
membrane, is quite different from that of true asthma, for in this 
case the difficulty is commonly in the entrance of air. The onset 
of the attack is usually sudden, and inspection will show that on 
inspiration the costal interspaces are greatly drawn in, as is also the 
epigastrium. There will be practically no signs in the chest which 
are not evidently due to the efforts at forced breathing, and a 
history of having had a foreign body in the mouth or of some 
laryngeal disease will usually be obtainable. Obstruction may, 
however, be present, and the history of a foreign body be absent 
in cases in which an abscess has burst into the air passages from 
the mediastinum or through the posterior pharyngeal wall. In 
such a case, however, there would be, in all probability, purulent 
expectoration. 

Laryngeal Spasm. — Laryngeal spasm producing difficult breathing 
causes symptoms precisely like those of a foreign body in the 
larynx, except that in spasm inspiration is accompanied by stridor, 
the cough is often constant and is very brassy or ringing. The 
patient will show by a gesture with his hand that the obstruction 
is in the larynx, if unable to speak. Such obstruction when seen 
in children is, as a rule, due to spasmodic croup, and, if so, prob- 
ably depends upon one of three causes, namely, laryngeal catarrh, 
rickets, or digestive disturbance. If in an older person, it is prob- 
ably due to aneurysm pressing on the recurrent laryngeal nerve, to 
a laryngeal crisis in locomotor ataxia, or to growths in the medias- 
tinum producing pressure on the nerve trunks going to the laryngeal 
muscles. Sometimes great enlargement of the peribronchial lymph 
nodes will cause reflex, laryngeal spasm. 



mam 



THE DIAGNOSIS OF RESPIRATORY AFFECTIONS 257 

Tumors of the Chest. — Tumors occur in the chest generally as 
mediastinal growths, and are most commonly sarcomas or lymph- 
adenomas. There will be found, if the growth be large, evidences 
of its pressure upon the chest wall, such as bulging and dulness on 
percussion over the swelling. This level of dulness is unaltered by 
changing the posture, as it is in pleural effusion. Generally there 
will be evidence of pressure on the bronchial tubes, which causes 
dyspnea, and of pressure on the thoracic vessels, which produces 
signs of impaired circulation as shown by cyanosis, venous engorge- 
ment, and flushing of the skin of the face and neck. Often such 
growths cause pleural effusions by pressure on the bloodvessels, 
or produce pulmonary consolidation or edema, by causing an 
exudation in the lung tissue. 

The diseased conditions from which it is necessary we should 
distinguish mediastinal growths during life are as follows: (i) 
Aneurysm; (2) abscess; (3) pleural effusion; (4) chronic pneumonia. 
There are several subdivisions of these diseases that might be made, 
but to all intents and purposes these are sufficient. Pericardial 
effusion may, perhaps, be named as the fifth lesion to be thought 
of. On general principles it may be said that primary mediastinal' 
growths are so rare that they can be excluded on this ground in 
many cases. 

Deeply seated aneurysm in the thorax is sometimes extremely 
difficult of absolute diagnosis from tumor, and but few rules can be 
laid down for its differential diagnosis from growths in the medi- 
astinum, for deeply seated aneurysm in this region cannot be said 
to possess any pathognomonic symptoms. The various portions of 
the aorta in which aneurysm occurs make its symptoms different in 
almost every case, and we are forced to rely more upon general 
conditions than absolute signs. Thus, if a patient has no direct 
symptoms of aneurysm, and none of those conditions present which 
we know predispose to such a lesion, such as atheroma of the blood- 
vessels, or syphilis, or a history of violent exertion or severe toil, 
we may with a certain degree of assurance look farther for symp- 
toms of mediastinal trouble of another sort than aneurysm. (See 
Aneurysm, in this chapter.) 

Unfortunately, the most common age for aneurysm is much the 
same as that for mediastinal disease, although mediastinal disease 
seems to occur more frequently in youth than does aneurysm, or 
in other words, is scattered over a wider range of years. The 
pain in some cases of aneurysm is often more violent than that 
of any other thoracic lesion except angina pectoris. If the 
aneurysmal sac be large enough to give a wide area of dulness on 
percussion, there may be an expansile movement. Hemoptysis is 
not in any way a differential sign, since in the one case it ma}' be 
due to aneurysmal leakage, and in another to ulceration of small 
17 



258 THE THORAX AXD ITS VISCERA 

bloodvessels by pressure exercised by a tumor, be it aneurysmal 
or malignant, or even benign. Aneurysm is relatively the more 
frequent lesion. (See latter part of this chapter.) 

Mediastinal abscess can be separated from mediastinal tumors 
with care. In the first place, in abscess we generally have a history 
of infection, or, if the case be one of cold abscess, it is commonly 
associated with a history of struma or spinal disease. If the abscess 
be acute, there is generally the history of pain, followed by a chill, 
more or less severe, and fever; or, if cold, then we frequently have 
irregular febrile movements, with long-continued ill-health and 
loss of flesh. Cold abscess, too, is generally in the posterior medi- 
astinum, while acute abscess generally occurs in the anterior space. 
Pulsation may frequently occur, owing to the transmission of the 
aortic or cardiac impulses. Mediastinal abscess is far more rare 
than aneurysm. 

THE HEART AND VESSELS. 

On attempting to study the heart sounds, we usually auscult the 
neighborhood of the apex beat and find, if the heart be healthy, two 
sounds, occurring one immediately after the other, which resemble 
"lub dup," the "lub" being the so-called first sound of the heart, 
produced by the contraction of the heart muscle and the tense 
valves, and the ''dup" being chiefly caused by the slapping to of 
the aortic valves. After listening in this region we next place the 
ear over the second right costal cartilage, in order to come as near 
as possible to the point of greatest intensity of the sound, produced 
by the aortic valves. If the heart is normal, we again find only 
the sounds, u lub dup," and nothing else. 

If the heart is feeble from exhausting disease, from fainting, or 
by reason of degeneration, we find that the sound "lub" is feeble, 
and the u dup" sound is also feeble, because the valves do not 
slap back into place with as much force as is normal. If, on the 
other hand, the heart is hypertrophied or stimulated, we find these 
sounds accentuated, and it is of importance to remember that 
marked accentuation of the aortic second sound, showing forcible 
closure of the aortic valves, indicates a condition of high arterial 
pressure, often the result of vascular spasm arising from chronic 
contracted kidney or general arterial fibrosis. On the other hand, 
if the pulmonary second sound at the third left intercostal space is 
accentuated, it indicates an increase in pulmonary pressure due to 
impediment to the flow of blood in the lungs. This pulmonary 
second sound is often markedly accentuated in both mitral ob- 
struction and regurgitation and in some cases of pneumonia and 
emphysema. 1 

1 By accentuation, I do not mean necessarily any increase in the loudness or 
volume of the sound, but an increase in its sharpness. 



THE HEART AND VESSELS 



259 




Fig. 86. — Showing the areas in which the various heart sounds are best 
heard in health. A is the area for the aortic valve; P, that for the pulmonary- 
valve; T, for the tricuspid valve; and M, for the mitral valve. The pulmonary- 
circle is a little high. 




Fig. 87. — Approximate positions of the valves of the heart. To the left the 
mitral, in the centre the pulmonary, to the right the tricuspid, uppermost the 
aortic. Compare with this the figure showing where the sounds of those valves 
are actually best heard (Fig. 86). 



260 THE THORAX AND ITS VISCERA 

The sound produced at the various orifices of the heart are heard 
best at or near the following points (Fig. 86), although the approxi- 
mate positions of the valves are shown in Fig. 87. The mitral 
valve is heard best at the apex beat ; the aortic valve at the second 
right costal cartilage, the tricuspid valve over the sternum on a 
line drawn from the third left intercostal space to the fifth right 
costal cartilage, and the pulmonary valve at the third left inter- 
costal space. 

All the heart sounds may be reduplicated in health and in 
disease. When the first sound is reduplicated, it is probably due 
to asynchronism of the two ventricles, whereby the first sound is 
split (lub-lub-dup) . This is sometimes heard in cases of very 
high arterial tension with chronic contracted kidney. When the 
second sound is doubled or split there is asynchronous tension of 
the two sets of sigmoid valves. Sometimes,, instead of a splitting 
of the first, or second sound, an additional or accessory sound is 
heard, which may be presystolic, or immediately after the first 
sound. In still other cases an accessory sound occurs in the 
middle of diastole. Splitting of the first sound is usually heard 
best over the base of the heart, whereas accessory or extra sounds 
are most audible in the apex. Sometimes reduplication of the first 
sound results from a pericardial adhesion, and in other instances 
the accessory presystolic sound is supposed to be due to a vigorous 
auricular systole. The exact significance of reduplicated and 
accessory sounds is not yet ascertained. If disease of the valves 
be present, we are apt to find reduplication of the second sound, 
as in cases of mitral stenosis, so that the sound is lub-dup-dup. 
This also occurs in pulmonary disease producing an abnormally high 
tension in the pulmonary circulation. Such reduplication is also seen 
in some individuals suffering from aortic stenosis. (See page 281.) 

Heart Murmurs. — Supposing that on listening to the heart in the 
mitral area — that is, in the neighborhood of the apex beat — there 
is heard in place of the normal sounds "lub dup," or with them, 
a murmur. What does it mean? It means that, friction sounds 
being excluded, either valvular disease, a relaxed mitral orifice, 
or marked anemia is present. Still more rarely the sound may be 
due to what is called a cardiopulmonary murmur, which may occur 
at any time in the cardiac cycle. This sound is produced not by 
the movement of the lung in the respiratory act, but by the move- 
ment of the lung by the action of the heart, a movement which 
occurs approximately seventy times a minute, instead of fourteen 
times, as it would if respiratory. The sound is produced, not in 
the heart, but by the displacement of air in the lung, and the 
murmur can often be arrested or altered in character by changing 
the posture of the patient. The fact that this type of murmur is 
heard still more clearly near the base of the heart, the absence of 



THE HEART AND VESSELS 261 

any signs of cardiac difficulty, such as are met in true cardiac dis- 
ease, and the fact that holding the breath on expiration or inspira- 
tion may stop the murmur, aid us in deciding that the murmur is 
one of the cardiopulmonary type, particularly as it is prone to be 
musical in character. 

The anemic murmur is particularly apt to be heard in the case 
of a feeble child, or, if in an adult, in association with other signs 
of disorder of the blood, which should make the physician suspect 
this condition to be the cause. Further than this, an anemic 
murmur is apt to be soft and purring, and associated with rather 
feeble heart sounds, probably due to the fact that the heart muscle 
is not well nourished; such a murmur will generally be found most 
marked at the left margin of the sternum near the third interspace. 
(See chapter on Blood.) 

Having found that there is a murmur, and having excluded the 
causes just named, it is now necessary to determine at what orifice 
of the heart it is produced, and the rule is to be remembered that a 
murmur is nearly always heard loudest at about its point of origin. 
We therefore place the ear over the aortic cartilage (second right). 
If the murmur be mitral in origin, it will not be heard at this 
place, unless it be so loud as to be transmitted from the apex. If 
it is aortic in origin, it will be louder here than at the apex. If it 
is tricuspid, it will be loudest in the tricuspid area; if pulmonary, 
loudest at the pulmonary area (Fig. 86). As murmurs at the 
tricuspid and pulmonary valves are rare, we nearly always have 
to deal with mitral or aortic murmurs, or both. In this way, 
therefore, we can determine the origin of the murmur, and that 
it is a mitral or an aortic murmur by determining its point of 
greatest intensity. 

Before attempting to differentiate the various murmurs in the 
heart it is to be distinctly understood that murmurs produced by any 
form of valvular lesion may exist with great intensity without there 
being any systemic disturbance or the patient being conscious of 
their presence. On the other hand, the murmur may be so faint 
as to be almost indistinguishable and yet the general symptoms of 
heart disease be very marked. This is because the development 
of general symptoms depends entirely upon the question of com- 
pensation by increased cardiac activity or hypertrophy. If 
there is a leak in a valve or constriction of an orifice, this leak or 
obstruction must be overcome by compensatory activity of the 
heart muscle. If the heart muscle can make up for the regurgi- 
tation or obstruction by increased effort, the circulation is unim- 
paired; but if it cannot do so, we have developed more or less 
rapidly, according to the lesion present and the condition of the 
heart muscle, characteristic symptoms. (See page 263.) 



262 



THE THORAX AND ITS VISCERA 



Mitral Murmurs. — Let us suppose that it is a mitral murmur. We 
must determine whether it is that of mitral regurgitation or ob- 
struction. 

It is likely to be that of mitral regurgitation, because this is the 
most common murmur heard in the heart; and if to this probability 
we add the fact that it is transmitted well into the axilla, and even 
heard at the angle of the scapula, our diagnosis is greatly aided, 
for this is the area of transmission of the murmur of mitral regurgi- 
tation (Fig. 89). The most important diagnostic point, however, 




Fig. 88. — Diagram modified from Page to show the relation of the various 
valves. A study of this diagram will render clear the time of the various cardiac 
murmurs. Thus in mitral regurgitation the blood passes back from the left 
ventricle to the left auricle during systole, and is dammed up in the pulmonary 
veins, the openings of which are seen in the left auricular wall, producing pressure 
on the pulmonary valves, the sound of which is thereby accentuated. 

is the discovery that the murmur occurs simultaneously with the 
first sound of the heart, or with systole — that is, with the apex beat 
or the carotid pulse. If it does, it is almost certainly one of mitral 
regurgitation. This murmur occurs with the first sound, or systole, 
because the ventricle in contracting drives most of the blood in the 
normal direction into the aorta, and also forces some of it back 
through the left auriculoventricular orifice into the auricle, causing 
a regurgitant murmur (Fig. SS). Sometimes there will be 
found in such cases a very marked accentuation of the second 
sound at the third left costal cartilage due to the increased pressure 



THE HEART AND VESSELS 263 

in the pulmonary vessels by reason of the distention of the auricle 
by the blood which regurgitates into it. The area of greatest 
intensity of the mitral regurgitant murmur is shown in Fig. 89. 

In adults inspection and palpation will rarely reveal much of a 
thrill over the precordium in mitral regurgitation, but in children 
this thrill is rarely absent and is often well marked. Often per- 
cussion will show that the area of cardiac dulness (see earlier part 
of this chapter) is broadened, extending beyond the right edge of 
the sternum and to the left of the mammillary line. 

In the diagnosis of the mitral regurgitant murmur the physician 
must not be misled by a loud aortic systolic murmur transmitted 
down the sternum to the area of the apex beat. 

If there is failure of compensation in mitral regurgitation the first, 
and one of the mOst prominent symptoms, is shortness of breath on 
exertion; the lips and ears do not possess their normal red hue, but 
are a little bluish; and if the congestion of the auricle and pulmonary 
veins is great, bronchitis may be constant or attacks of hemoptysis 
may develop. Palpitation of the heart will also be complained 
of; and if the patient has developed the lesions in early life, the 
finger tips are apt to be clubbed. If the failure of compensation is 
more complete, all these symptoms become more marked, and the 
shortness of breath even when lying down, becomes most dis- 
tressing; indeed, the patient may be comfortable only when 
sitting up. Dropsy of the lower extremities now comes on; the 
liver becomes enlarged from portal congestion, due to back pressure 
in the vessels of the lungs and in the right side of the heart. This 
results in disordered gastric digestion by reason of the catarrh of 
the stomach which ensues, and the urine becomes albuminous, not 
necessarily from any true renal lesion, but as the result of engorge- 
ment of the kidneys with blood, partly the result of poor arterial 
flow and partly because of venous stasis. 

If the murmur is due to mitral stenosis, it will be found that 
it does not occur with systole, but just before it; in other words 
it is presystolic in point of time (Figs. 89 and 90), and is not 
transmitted into the axilla but to the right, to the midsternal 
line. This murmur occurs before systole, or the first sound, 
because it is produced by the blood passing through an obstruc- 
ted left auriculoventricular orifice, and, as the ventricle does not 
contract (systole) until it is filled, the murmur is made while 
it is filling, and so is presystolic. 

This presystolic murmur is not prolonged, but short and brief, 
and seems to rise in crescendo until it merges into the first sound. 
In other cases a long drawn-out, all- the-way- through, diastolic 
murmur is heard merging finally into the crescendo at the begin- 
ning of the first sound. It is due to the same cause. Sometimes 
a third sound occurs at the beginning of diastole which is short 




Fig. 89. — Showing at x the apex beat where the murmurs of mitral regurgita- 
tion and obstruction can be best heard. The arrow pointing to the axilla indicates 
the direction in which the regurgitant murmur is transmitted, and the arrow- 
pointing to the sternum the direction of transmission of the obstructive murmur. 




Fig. 90. — MO shows area of greatest intensity of a mitral obstructive murmur. 
The fine lines indicate the area in which is felt the characteristic diastolic thrill 
of mitral stenosis. 



M 



THE HEART AND VESSELS 265 

and supposed by some to be due to closure of the stiffened mitral 
leaflets. The first sound of the heart is short and snapping over 
the apex but to the right, over the right ventricle, it may be nearly 
normal in length. Palpation and inspection of the apex beat also 
reveals a short or quick impulse often preceded by a brief thrill 
due, it is thought, to the projection of the auricular stream of 
blood against the anterior ventricular wall. Over the area from 
the third to the fifth rib there is systolic retraction of the inter- 
spaces due to the enlarged right ventricle being drawn away from 
the chest wall in systole. In the second left interspace near the 
sternum there may be a systolic impulse due to the hypertrophied 
right ventricle driving the blood forcibly into the pulmonary 
artery, and if the ear is placed over the third right interspace, it 
will hear an accentuated pulmonary second sound due to the back 
pressure of blood from the distended and obstructed left auricle. 
A shock may also be felt at this point. The action of the heart 
may be quite slow but commonly it is rapid. 

If the patient has a tumultuous action of the heart, with disap- 
pearance of the long-drawn-out or short presystolic murmur, this 
indicates that the left auricle is tired out or dilated in endeavoring 
to force the blood through the narrowed orifice. This results in 
in still further back pressure on the pulmonary valves, so that 
their sound is sharpened. Dyspnea, bloody spitting, pulmonary 
congestion, enlargement of the liver and edema of the extremities 
are now developed. The back pressure may become so great that 
the right ventricle becomes dilated and the tricuspid valves leak, 
so that there is a regurgitant murmur at this orifice with pulsa- 
tion of the jugular veins and of the liver. 

The great irregularity of the apex beat is due to irritability 
of the left ventricle, which does not receive its proper quota of 
blood, and to the fact that the contraction waves arising at the 
sino-auricular node are prevented from passing along the auricular 
wall and across His' auriculoventricular bundle in part or com- 
pletely. When this occurs the ventricle contracts on its own 
initiative and does not follow auricular contraction as it should, 
the lesion at the base of the mitral leaflets having gone deeply 
enough to nip His' bundle. The auricular rate as seen in the 
jugular bulb may be as high as 140 per minute, whereas the apex 
beat may be as low as 40 if the block is complete. The difficulty 
with which the ventricle is filled by the auricle combined with 
the lack of sequence in the action of the auricle and ventricle 
causes great variations in the regularity and volume of the pulse 
wave. When the auricle is so fatigued or dilated that it ceases 
to contract it simply acts as a fibrillating pouch through which 
the blood passes from the pulmonary veins. Complete heart 
block or the sudden development of auricular fibrillation may 



2 66 



THE THORAX AND ITS VISCERA 



cause sudden death, but often life is preserved for a long time, 
particularly in cases of fibrillation of the auricles. (See Chapter 
on Pulse and Bloodvessels, and Blood-pressure.) 

In the diagnosis of mitral obstruction the physician must not be 
misled by the possible presence of what is known as Flint's murmur, 
a presystolic murmur heard in the mitral area, and due to relaxation 
of the mitral valves, which are thrown into vibration during diastole 
by blood regurgitating from the aorta in aortic regurgitation. 

Aortic Murmurs. — If, however, we have found the murmur to be 
aortic in origin, we must determine whether it is that of aortic 
regurgitation, aortic roughening, aortic obstruction, or aneurysm. 
Aortic obstruction or roughening is so common in persons of advanced 
years that it must be excluded from the diagnostic possibilities 
before any further steps are taken. In young persons it is com- 
paratively rare, particularly if they are children. 





t 

Fig. 91. — Showing the area of Fig. 92. — Showing the area in 

greatest intensity and the direction of which the murmur of aortic regurgi- 

transmission into subclavian and tation can be most clearly heard. The 

carotid arteries of the aortic obstruc- left nipple is raised by the position of 

tive murmur. the arm. 

This murmur occurs with the systole of the ventricles, the 
carotid pulse, and apex beat; it is harsh, as a rule, and is trans- 
mitted up into the carotid, and it may be into other arteries of 
less importance (Fig. 91). It is produced by the contraction of 
the ventricle driving the blood through a narrowed or roughened 
aorta or aortic orifice. A similar murmur may arise from vege- 
tations on the aortic valves. Considerable hypertrophy of the 



THE HEART AND VESSELS 267 

left ventricle is usually produced, and the apex beat is strong, 
forcible, and displaced to the left if compensatory hypertrophy is 
present. 

As a matter of clinical fact, true aortic obstruction, due to vege- 
tations on or contractions of the aortic valves themselves, is always 
associated with a certain degree of aortic regurgitation, even 
though the regurgitant murmur may not be discoverable. Aortic 
systolic murmurs entirely free from any aortic regurgitation are 
really due in the great majority of cases to aortic roughening 
produced by atheromatous plaques on the aortic wall. 

If compensation fails in aortic obstruction, which is rare, the 
symptoms are much like those resulting from mitral regurgita- 
tion, but in addition there are apt to be present early in the 
process of failing compensation, some lightness of the head, dizzi- 
ness or vertigo, or faintness, owing to a deficient blood supply to 
the brain. Very commonly, too, it will be found that in associa- 
tion with the aortic stenosis there also exists aortic regurgitation, 
which is chiefly responsible for the symptoms presented. Dropsy is 
very rarely seen in patients with aortic stenosis. On the contrary, 
they present, as a rule, the lean and poorly nourished appearance 
so often found in the adult, well advanced in years, who has 
atheromatous tendencies in the bloodvessels. 

If the murmur is aortic and occurs after the systole, or the apex 
beat, the murmur is that of aortic regurgitation, and is called the 
diastolic aortic murmur. It is heard loudly at the aortic cartilage 
(second right), often equally marked to the left of the sternum, and 
it is transmitted down along the sternum very clearly and into the 
left ventricle, so that it is plainly heard at the apex (Fig. 92). In 
this condition we have usually marked dilatation of the heart with 
hypertrophy (the so-called " ox-heart"), and a peculiar trip-hammer 
pulse (see chapter on Pulse), sometimes called the "water-hammer" 
or Corrigan pulse. This murmur is due to incompetence of the 
aortic valves, which allow the blood to regurgitate into the heart 
after it is driven out into the aorta. If in association with this 
murmur we rind displacement of the apex beat downward and to 
the left, with extension of cardiac dulness to the right, the " water- 
hammer" or "trip-hammer" or "Corrigan pulse," the throbbing 
arteries, and capillary pulsation in the skin and mucous membranes 
the diagnosis is assured. The capillary pulse (Quincke's pulse) is 
best developed by drawing the thumb nail sharply across the 
forehead, thereby causing a red mark, which can be seen paling 
and flushing with each beat of the heart (Quincke's sign), or by 
pressing a glass slide on the inner part of the lower lip, when 
the same capillary pulsation will be found. Ophthalmoscopic 
examination will often reveal similar pulsation of the retinal 
arteries. (See chapter on Pulse and Blood-pressure.) 



268 THE THORAX AND ITS VISCERA 

The development of ruptured compensation in aortic regurgi- 
tation presents more typical general systemic symptoms than any 
of the ordinary valvular lesions of the heart. In addition to 
headache, vertigo, and a tendency to syncope associated with 
palpitation and a sense of cardiac oppression, we often have a 
great deal of cardiac pain, of a dull, aching character in rare 
instances, but more often intensely sharp and lancinating, often 
darting down the left arm, particularly at night. The dyspnea is 
often extreme, the patient suffering from terrible attacks of short- 
ness of breath and often sitting day and night in a chair with his 
head resting on the back of a chair placed in front of him. As 
time goes on the constant struggling for breath exhausts him, and 
he falls asleep, only to wake in a few moments gasping for air. 

Tricuspid Murmurs. — If the examination has shown that the mur- 
mur is loudest in the tricuspid area, it is to be remembered that in 
the vast majority of cases the condition is one of tricuspid regurgi- 
tation, for tricuspid stenosis is an exceedingly rare lesion. The 
time of the murmur of tricuspid regurgitation is identical with 
that of mitral regurgitation (systolic), because the tricuspid 
valves are, functionally speaking, the counterpart in the right 
side of the heart of the mitral valves in the left. (See Fig. 88.) 

This murmur is best heard in Fenwick's triangle, the base of 
which extends two inches to the right of the sternum on the line 
of the sixth chondrosternal articulation, the apex of the triangle 
being at the level of the fourth chondrosternal articulation. (See 
Fig. 86.) 

Pulmonary Valvular Murmurs. — Actual disease of the pulmonary 
valves is exceedingly rare, and is usually congenital; pulmonary 
regurgitation is almost never met with. The signs of pulmonary 
stenosis due to congenital defect are cyanosis, hypertrophy of the 
right ventricle, a systolic murmur at the left side of the sternum, 
which is not transmitted upward, and a weak pulmonary second 
sound. 

The murmurs sometimes heard, and the thrills sometimes felt, in 
the area of the pulmonary valves are generally due to anemia, the 
puerperal state, or some neurosis, and only rarely to congenital nar- 
rowing of the pulmonary artery, or to compression of the vessel 
by the heart. If the last two causes are present, the ventricular 
septum is usually deficient and cyanosis is noticeable. 

The following rules, laid down by Hochsinger, may be used for 
making the diagnosis of congenital cardiac disease. 

i. In childhood loud, rough, musical heart murmurs, with normal 
or slight increase in the heart dulness, occur only in congenital 
heart disease. The acquired defects with loud heart murmurs in 
young children are almost always associated with great increase 
in the heart dulness. 



THE HEART AND VESSELS 269 

2. In young children heart murmurs, with great increase in the 
cardiac dulness to the right and feeble apex beat, suggest congenital 
changes. The dulness to the left is only slightly altered. On the 
other hand, in the acquired endocarditis in children, the left heart 
is chiefly affected and the apex beat is visible; the dilatation of the 
right heart comes late and does not materially change the increased 
strength of the apex beat. 

3. The entire absence of murmurs at the apex, with their evident 
presence in the region of the auricles and over the pulmonary 
orifice, is always an important element in differential diagnosis, 
and points rather to septum defect or pulmonary stenosis than to 
endocarditis. 

4. An abnormally weak second pulmonic sound associated with 
a distinct systolic murmur is a symptom which, in early childhood, 
is to be explained only by the assumption of a congenital pulmonary 
stenosis, and possesses, therefore, an importance from a point of 
differential diagnosis which is not to be underestimated. 

5. Absence of a palpable thrill, despite loud murmurs which are 
heard over the whole precordial region, is rare, except with con- 
genital defects in the septum, and it speaks therefore against an 
acquired cardiac affection. 

6. Loud, especially vibratory, systolic murmurs, with the point 
of maximum intensity over the upper third of the sternum, associ- 
ated with a lack of marked symptoms of hypertrophy of the left 
ventricle, are very important for the diagnosis of a persistence of 
the ductus Botalli (ductus arteriosus), and cannot be explained by 
the assumption of an endocarditis of the aortic valve. 

Pericardial Friction Sound is heard best at the base of the heart — 
that is, at about the third rib. It is separated from pleural friction 
by its frequency and by the fact that it continues when the patient 
holds his breath. (See Fig. 93.) 

Laennec likened this friction sound to the noise made by the 
leather of a new saddle when used for the first time. Sometimes it 
sounds like the crunching of dry snow under the shoe. It is usually 
a to-and-fro sound. 

Aortic Aneurysm. — Because the murmurs of aneurysm of the 
aorta may be mistaken for those due to valvular lesions they are 
considered here. The characteristic symptoms of aortic aneurysm 
vary greatly with the site of the lesion. The most typical signs 
are a "bruit" or angry murmur, systolic in point of time, with 
a thrill over the growth, dulness on percussion over the area of 
this thrill, dyspnea, pain, cardiac hypertrophy, and functional dis- 
turbance of the heart. It is to be remembered that small aneurysms 
deeply situated, which do not press upon organs, may produce no 
symptoms for years, and finally be discovered only at autopsy. 

Let us suppose that a patient presents himself with great 



270 



THE THORAX AND ITS VISCERA 




Pig. 93. — Area in which pericardial friction sound is best heard. 




Fig. 94. — Case of aortic and innominate aneurysm, with erosion of the clavicle 
and ribs from the author's wards in the Jefferson Medical College Hospital. 
This case is of extraordinary interest because this picture was taken thirty-five 
months after an arrest of the growth of the aneurysm by electrolysis. 



THE HEART AND VESSELS 27 1 

engorgement of the vessels of the head and neck and arm of 
the right side, with perhaps edema of that arm. The heart 
may be pushed downward and to the left and the voice may be 
lost or partially impaired by pressure on the recurrent laryngeal 
nerve of the right side. The pupil of the eye may be widely 
dilated through irritation of the sympathetic, and there may be 
unilateral pallor of the face from this cause. If the pupil is con- 
tracted, then the ciliospinal fibres are paralyzed by pressure. In 
such a case pain is apt to be a prominent symptom and so severe 
as to be almost like that of true angina. Percussion over the 
second right interspace will give impaired resonance, and auscul- 
tation of the area of the pulmonary valves may show a pulmonic 
systolic murmur, due to pressure on the pulmonary artery, which 
in turn causes hypertrophy and dilatation of the right ventricle. 
There may be bulging of the first, second, or third interspace on 
the right side. Generally such symptoms will be due to an aneurysm 
of the greater curvature of the ascending aorta, although they may 
be due to a tumor in the anterior or middle mediastinum; but the 
expansile pulsation, the bruit, and the history of the case will 
usually make the differentiation possible. 

Again, let us suppose that the patient has a ringing, brassy cough, 
difficulty in swallowing, and expansile pulsation in the episternal 
notch and epiclavicular space of the left side, and dulness on per- 
cussion over the first and second left intercostal spaces. The left 
side of the face and neck may be engorged from pressure on the left 
innominate vein. Pupillary symptoms similar to those already 
named may be present. There is difficulty in breathing, particularly 
on inspiration, owing to the pressure of the growth on the trachea, 
the paralysis of the left vocal cords, and the pressure on the left 
bronchus, and there is dysphagia due to pressure on the esophagus. 
The voice is altered from paralysis of the vocal cords due to pres- 
sure on the left recurrent laryngeal nerve. (See Fig. 95.) These 
symptoms indicate a lesion of the transverse arch. 

If, however, none of these important signs are present anteriorly, 
we must search for some of them posteriorly, particularly the bruit 
and the expansile pulsation, and if these are found to the left of 
the vertebral column near the angle of the scapula, we can rest 
assured that the aneurysm involves the descending aorta. Severe 
intercostal pain is often felt in these cases. 

In this connection it is well to recall the fact that aneurysm of 
the ascending portion of the aortic arch is by far the most common 
condition. Out of 953 cases of aortic aneurysm, analyzed by my- 
self and one of my former assistants, Dr. Holder, no less than 570 
were situated in the ascending part of the arch; of these, 544 were 
sacculated and 26 fusiform. Aneurysm of the transverse arch 
occurred 104 times,Jand of the descending part no times. Of the 
544 cases, 400 were in males. 



272 



THE THORAX AND ITS VISCERA 



There are other symptoms connected with aneurysm which should 
not be overlooked. The first of these is "tracheal tugging," a sign 
which is found in some cases but not in all. The patient being in 
the erect position, the ringers of the physician grasp the cricoid 
cartilage and gentle upward traction is produced. When aneurysm 
is present, a distinct tug will be felt with each beat of the heart. 
It is important for us to remember, however, that this sign of 
aneurysm is rarely met with and is not pathognomonic, for, as 




Fig. 95. — A posterior view, showing how an aneurysm of the transverse 
aorta presses on the recurrent laryngeal nerve. The cut shows the relation of 
the aorta, where it is surrounded by the loop of the recurrent nerve, to the left 
bronchus and the lower part of the trachea. A, aorta; P, pneumogastric nerve; 
R, recurrent nerve; L, larynx. (Dieulafoy.) 

Sewell has pointed out, it may occur in patients who have adhe- 
sions in the left pleural sac or diminished extensibility of the lung, 
or both combined. Further, in healthy persons the descent of the 
heart with the diaphragm on deep inspiration may press the aortic 
arch on the left bronchus, and so transmit to the trachea a tug 
not due to aneurysm. Another sign is the loss of pulsation in the 
peripheral vessels, the result of the loss of the heart's impulse in 
the aneurysmal sac. 

Doubtful cases of aortic aneurysm should be subjected to the use 
of the radiograph and nuoroscope, since this will often reveal the 



THE HEART AND VESSELS 273 

growth, particularly if the sac contains a firm clot. The exami- 
nation should be lateral as well as anteroposterior to determine the 
exact position and direction of the growth. 

Dilatation and Feebleness of the Heart. — Entirely apart from 
valvular lesions we have a number of other causes which seriously 
disturb the action of the heart and the general circulatory condition. 
The first of these is dilatation of the heart, independent of associ- 
ated valvular disease. Let us suppose that a man presents himself 
with a history of shortness of breath on exertion, so great that 
his activities are greatly reduced and his usefulness impaired. He 
gives a history that he was well until he made some extraordinary 
exertion. Since that time his symptoms of heart failure have been 
marked. He may have attacks of syncope. Examination of his 
heart reveals on inspection a diffuse thrill in the region of the 
apex; but this thrill is too feeble to be felt, though well marked 
to the eye if his chest is thin. Percussion shows that the area of 
cardiac dulness is increased vertically and laterally, and ausculta- 
tion will discover feeble heart sounds. If the dilatation of the 
heart cavities is associated with dilatation of the orifices, a mur- 
mur may be present, most commonly that of mitral regurgitation, 
without there being in association any actual disease of the mitral 
valves. Sometimes tricuspid regurgitation is also found. The first 
sound, before it becomes very feeble, may be short and flapping 
like the ordinary second sound. Marked arrhythmia of the heart 
is often present. 

The influence of severe strain in producing cardiac disease 
deserves careful study on the part of the physician. The study 
can be divided into three parts: The condition of the heart im- 
mediately after acute overstrain, the condition after chronic over- 
strain, and the final condition often met with months or years 
after the strain. 

It is now well known that immediately after severe muscular 
effort an examination of the heart will often reveal in entirely 
healthy persons a distinct increase in the area of cardiac dulness, 
and,' not infrequently, a murmur which disappears with rest. 
The increase in the area of dulness is, of course, due to more or 
less cardiac dilatation and the murmur to the same causes, since 
the dilatation results in stretching of the circular muscular fibres 
governing the mitral or tricuspid orifices, so that even if the valves 
be healthy they cannot close the orifice (Fig. 96). In some cases 
this action seems to be in the nature of a safety valve, in others 
a sign that the heart has been unduly strained. In the first class 
the murmur disappears at once or very shortly after the exertion 
ceases; in the other case it persists until after a long period of rest, 
when the heart has had a chance to recuperate and regain its 
normal tone. Persons having the latter condition ought to be 
18 



274 THE THORAX AND ITS VISCERA 

advised against severe forms of exercise, particularly if they are 
old in actual years or prematurely aged. 

Closely associated with these patients is that class who suffer 
from prolonged feebleness of the heart after an attack of true 
influenzal infection, a feebleness which may last for many 
years. Where there is a history of previous cardiac difficulty 
there can be little doubt that the poison of this malady magnifies 
it and produces far too often a permanent increase in the disease. 
In other instances where the heart is primarily healthy the con- 
dition is usually a fleeting one, although it is not to be forgotten 
that undue muscular activity on the part of the patient soon after, 
or during, an attack of influenza may be provocative of permanent 
cardiac incompetency. 



Pulmonary valves. 



,1...,..; Hj, V Aortic valves. 



/ 

/ 
i 

Mitral valve. "/~~ 



Tricuspid valves. 



Left ventricle. ——_—--' 

Right ventricle. 

Fig. 96. — The dotted lines show the dimensions to which the heart and its 
orifices increase in diastole, and in pathological dilatation this may be permanent. 
(Modified from His and Spalteholz.) 

Such patients often suffer from faintness and precordial dis- 
tress on exertion, and physical examination usually reveals a 
feeble and distant first sound, and a second sound lacking in tone 
because of lack of force in the systole of the heart. They also 
have edema of the lower extremities, sometimes a more or less 
decided trace of albumin in the urine, but no casts unless there be 
associated renal lesions, the albuminuria being due to stasis in 
the kidney. They are often pallid and relaxed, and need rest and 
hydrotherapeutic measures more than the internal use of drugs. 
Such patients, too, particularly if they are advanced in years, 
not rarely progress rapidly into a gradually increasing circulatory 
feebleness and so to death. 



THE HEART AND VESSELS 275 

There is another heart condition closely allied to that just 
described, at least in one sense, namely, the feeble heart of tuber- 
culosis. Too little attention is paid to this organ in this disease, 
probably because the mind is centred upon the lungs. 

Hypertrophy of the Heart. — Hypertrophy of the heart rarely 
occurs in persons without valvular lesions, sometimes as the result 
of excessive and severe toil. It is seen most commonly by the author 
in medical students, who, during their holidays, devote their time 
to severe athletic sports, or to much manual labor, and who, on 
leading sedentary lives in the winter, develop irregular cardiac 
action, palpitation, and some shortness of breath. Examination 
of the precordium in such cases shows a forcible impulse of the 
apex of the heart against the chest wall, some bulging of the chest 
wall if the hypertrophy be very great, and no murmurs, but in 
their place heart sounds very much louder than normal. Palpation 
shows the apex beat to be lower than normal, and on percussion 
an increase in the area of cardiac dulness is also found. Hyper- 
trophy not dependent upon a valvular lesion or vascular disease 
with high tension has little significance. 

Cardiac Arrhythmia. — Again, let us suppose that a patient 
presents himself with the statement that he has attacks in which 
he suffers from a very rapidly beating heart. His skin is alternately 
red and pale, and sweats without cause, but a careful examination 
of the heart fails to reveal any murmurs or organic abnormality. 
There are considerable shortness of breath on exertion and marked 
palpitation and arrhythmia. Such a case may be suffering from a 
condition in which there is some deficient action of the pneumo- 
gastric nerve, whereby the heart is not properly controlled, or the 
irregular cardiac action may be due to sudden vasomotor relax- 
ations, which by dilating the blood paths reduce the normal arterial 
resistance. (See chapter on Blood Pressure and Pulse.) This is 
a condition seen in association with some neuroses and very 
commonly met with in young persons who use tobacco to excess. 
The symptoms of the so-called "tobacco heart" are indeed chiefly 
those of arrhythmia due to pneumogastric and vasomotor disorders. 

An exceedingly irregular arrhythmical action of the heart coming 
on in the course of an acute infectious disease, or 'in any state pro- 
ductive of sepsis, points to the possibility of the patient having an 
embolism or thrombosis of one of the coronary arteries. If the 
vessel is suddenly plugged, death occurs; but if the process is 
gradual, necrosis or a white infarct is produced. Often the infection 
causes a degenerative change in His' bundle whereby the impulses 
are partly or completely blocked. 

Bradycardia. — Rarely because of irritation of the vagus nerves 
or centres a state of bradycardia develops, in winch the heart beats 
very slowly, perhaps only thirty or even as slowly as twelve times 



276 THE THORAX AND ITS VISCERA 

a minute. (See Stokes- Adams Disease.) Bradycardia, or great 
slowness of the heart, may be due to a neurosis of the vagi, and 
also occurs in some infectious diseases. It is also seen in jaundice. 

Tachycardia. — One of the most common causes of tachycardia, 
or rapid heart, is exophthalmic goitre, in which condition we have 
not only exophthalmos and enlargement of the thyroid gland, but, 
in addition to the tachycardia, a marked thrill over the carotid 
arteries, in which vessels a purring murmur of considerable in- 
tensity can often be heard. The patient usually suffers from 
considerable nervous excitement or mental depression. Tachy- 
cardia is also met with in neurotic persons, and in these cases it 
usually occurs in paroxysms. 

Heart Block and Stokes-Adams Disease. — When a patient 
suffers from attacks of extremely slow pulse with vertigo, syncope, 
apoplectiform or epileptiform seizures, associated with pulsation 
of the veins of the neck which is often far more frequent per 
minute than the beat of the ventricle, the condition is called the 
" Stokes-Adams syndrome." This incoordination of the auricles 
and ventricles is due to disease of the auriculoventricular muscle 
bundle of His. Graphic tracings of the apex beat, the radial 
pulse, and the jugular beat, showing this incoordination may be 
made by the use of the multiple sphygmocardiograph of Jacquet. 
(See Fig. 101.) (See chapters on Pulse, Bloodvessels, and Blood- 
pressure.) 

Fatty and Feeble Heart. — Before discussing the signs of so-called 
fatty heart we must decide what is meant by this term. True 
fatty heart — that is, that condition of the heart in which this 
organ has undergone true fatty degeneration — has no pathog- 
nomonic signs, so far as the heart itself is concerned. In these 
instances we base our diagnosis upon the presence of fatty de- 
generation of the more superficial organs, such as the arcus senilis 
in the eye, 1 the presence of atheromatous bloodvessels, the feeble 
heart sounds at all times, and the evident feebleness of the heart 
on exertion. The history of poisoning by any one of the poisons 
causing fatty degeneration is also to be sought after in some cases. 
Marked fatty degeneration is often present in cases of pernicious 
anemia. It is not possible to make a differential diagnosis from 
the physical signs between fatty and fibroid heart. 

Another state quite distinct from true fatty heart, but with some- 
what similar symptoms, is seen in cases in which an excessive 
amount of fat has been deposited around the heart and between 
its fibres as well as in or around the other organs of the body. 
Here there is little or nothing the matter with the heart muscle, 
except that it is overloaded with a weight of fat. 

1 Ophthalmologists and many clinicians deny that arcus senilis has any signifi- 
cance of this character. (See chapter on the Eye.) 



THE HEART AND VESSELS 277 

When a man shows signs of general degenerative changes, has a 
feeble heart, some dyspnea, and perhaps some edema of the lower 
extremities, without valvular disease, we may conclude that he has 
degenerative myocarditis. Valvular disease may, of course, be found 
associated with the myocardial lesion. Such cases make up the 
greater number of sudden deaths, called popularly " death by 
sudden cardiac failure," the end being due to sudden dilatation 
or strain. 

Great feebleness of the heart and of the general system, loss of 
flesh (or sometimes maintenance of weight), and pigmentation of 
the skin and buccal mucous membranes point strongly to Addison's 
disease. (See chapter on the Skin.) 

Sudden attacks of cardiac feebleness sometimes come on as 
cardiac crises in locomotor ataxia and in glossolabiopharyngeal 
paralysis. 



CHAPTER IX. 
THE PULSE, BLOODVESSELS, AND BLOOD-PRESSURE. 

Feeling and counting the pulse — The condition of the bloodvessels on palpation — 
The quality, force, tension, and volume of the pulse in health and disease — 
Blood-pressure in health and disease. 

The Pulse.— One of the first things that the physician does when 
he is studying the condition of a patient is to count the pulse, 
even if the symptoms which are present do not indicate circulatory 
disturbance, because the pulse is an index of the condition of the 
heart as to its power, its valvular action, and its nervous state, and 
also because any acute or chronic disease in the various parts of the 
body are prone to cause changes in the circulatory state. Emotional 
conditions also alter it. The pulse very often gives information 
of the presence of renal disease, and it will frequently give a general 
idea of the tone or degree of debility of the patient. By feeling 
the pulse we also gather valuable information as to the condition 
of the arteries, and this is a very important part of the diagnosis, 
for, to use an old saying, "A man is only as old as his arteries;" 
and if he is sixty years of age and has good vessels, he is, as a rule, 
younger in health than another man of thirty with bad vessels,- 
because it is by the bloodvessels that the tissues of the body are 
nourished, and, as life depends upon this process of nutrition, the 
better the vessels the better the vitality. 

When counting the pulse of a patient who is well enough to 
be up and about, the physician should wait until sufficient time 
has elapsed after exercise for the pulse to become quiet, and the 
patient should be in a sitting or reclining posture in order to prevent 
overaction of the heart. This is particularly important in the case 
of nervous individuals. An entirely erroneous conception of the 
circulatory state may be reached if this precaution is ignored, and 
it is well to insist on perfect rest in bed for several hours prior to 
the examination in grave cases. After the character of the pulse 
is taken at rest it may be taken after exercise. 

Often when called to see a sick child or nervous woman, who 
may be sleeping at the moment of the physician's arrival, a true 
estimate of the pulse can be made without disturbing the patient 
by gently putting the tip of the finger on the temporal artery 
where it passes over the zygomatic process. This is of consid- 
erable importance, because in some patients the excitement of 



THE PULSE 279 

the doctor's visit may produce marked alterations in pulse rate. 
This artery may also be used for this purpose in cases of tremor, 
chorea, delirium, or mania, in which the hand is constantly moved 
about so that the radial pulse cannot be counted. 

In counting the pulse it is best to count it for the entire minute, 
or to count it for fifteen seconds and then multiply the result by 
four to get the per minute rate. If the pulse is irregular, it is 
always best to count it for a minute. If the pulse is very irregular 
and running, and so difficult of counting, the estimate should be 
made by Hstening at the precordium for the apex beat. Further- 
more, it not infrequently happens when there is disorder of the 
heart due to drugs or lesions, such as defects in His' bundle, the 
pulse at the wrist may give a much slower rate per minute than 
the actual cardiac beat because some of the impulses caused by 
systole fail to reach the wrist. The pulse rate at the wrist in such 
cases is therefore not identical with the actual heart beat per 
minute, and no pulse rate should be considered accurately recorded 
unless controlled by ausculting the heart beat as well." 

The pulse varies widely as to volume, character, rapidity, and 
force, within normal limits, and still more so under the effects of 
disease. It also varies greatly according to age. Thus, the pulse 
of the newborn child is usually about 135 to 140, at one year 120 
to 130, at two years 105, at four years 97, at ten years about 90, at 
fifteen 78, and from twenty to fifty years about 70 per minute. At 
eighty years of age it is usually about 80 beats per minute. The 
rate is also increased by taking food, by exercise, by nervousness, 
and by pain and fever. 

The volume of the pulse wave depends chiefly upon the quantity 
of blood expelled from the heart at each systole, and also upon the 
condition of the aortic valves of the heart, insofar as their ability 
to prevent regurgitation is concerned. Irritation of the vagus 
nerves usually results in a large pulse wave, as does also cardiac 
hypertrophy. If, on the other hand, part of the blood thrown out 
of the heart into the aorta falls back into the ventricle (aortic regurgi- 
tation), we have a pulse which is called, because of the peculiar 
sensation which it gives to the finger, "trip-hammer," " water- 
hammer," or " Corrigan's pulse" (Fig. 99). In such a case, because 
of the power of the ventricle, the blood is forced out into the 
aorta with great force, but as the last part of the wave regurgi- 
tates the pulse is found- to be short and sharp. In mitral regur- 
gitation, and particularly in mitral stenosis, the pulse is usually 
small in volume, because the left ventricle has not, or cannot get, 
enough blood at each beat to send out a voluminous wave into 
the aorta. (See Fig. 100.) 

In other instances the beat of the pulse may be described as 
small and quick without meaning that it is rapid. In the infec- 



280 THE PULSE, BLOODVESSELS, AND BLOOD-PRESSURE 

tious fevers the arterial wall may feel relaxed, almost like that of 
a distended vein, and the pulse wave seem large, yet the pressure 
is low and the heart beat usually rapid. So, too, in the later stages 
of severe cardiovascular disease there often develops a relaxed 
state of the arterial wall, in place of the hard and resistant wall 
felt in the earlier stages of the disease, probably because the 
muscular coat of the vessel like the muscle fibres of the heart, has 
undergone degeneration. 

So far as the character of the pulse is concerned, we recognize 
one which is slow and full, as that seen after digitalis is used; that 
which is short and sharp, as in aortic regurgitation; that which is 
small and hard, as is often seen in aortic obstruction, and the 
small, wiry pulse of acute peritonitis. 

The force and rapidity of the pulse also depends largely on the 
condition of the bloodvessel walls, particularly the rapidity. The 
rapidity also is influenced by the activity of the pneumogastric 
nerves in regulating the speed of the heart. If the arterial pressure 
be very high, through spasm of the arterioles, the difficulty experi- 
enced by the heart in forcing blood into the arteries will be so great 
that pulsation may be very slow, whereas if the normal resistance 
to the action of the heart be removed by vascular relaxation, the 
beat will be rapid, just as the wheels of a locomotive fly around on a 
slippery track when the friction or resistance is removed. If the 
vessels are relaxed, the impetus communicated to the column of 
blood in the vessels by the heart is lost, and so the pulse is not 
forcible; or if the resistance is excessive, the force is dissipated. 

A rapid pulse is seen most commonly as the result of stimulation 
of the heart by drugs, by paralysis of the vagi by drugs, by fever, 
or by fear. Fear causes the vagus to lose control of the heart, 
and fever acts by reason of the stimulant effect of heat upon this 
viscus and its depressant effect upon the vagus. In other words, 
the quick pulse of fever is not a mere coincident symptom of 
fever, but the result of it. As a symptom of organic disease it is a 
frequent manifestation of exophthalmic goitre. Often in this con- 
dition the pulse becomes so fast that it cannot be counted. In 
all cases of great prostration and feebleness a very rapid pulse is 
present. 

Great force of the pulse is due to hypertrophy, or overaction of 
the heart because of stimulation; and great feebleness is generally 
caused by marked dilatation not associated with hypertrophy, by 
chronic myocardial degeneration, and in acute disease by exhaustion 
of the heart muscle or acute myocardial degeneration. 

Various names are applied to a pulse possessing certain peculiari- 
ties. Thus, we have under the name pulsus paradoxus a pulse which 
disappears with each deep inspiration. It is usually due to indura- 
tive mediastinopericarditis, whereby inflammatory bands press on 



THE PULSE 28l 

the bloodvessels or the heart or suction ensues when large vessels 
are drawn upon. If the beats of the heart are irregular in force 
or volume, but regular in rhythm, we have developed what is called 
a pulsus alternans. Sometimes such a pulse is due to extra-systoles. 

Extra-systoles occur, as a rule, by reason of the fact that con- 
traction waves arise in other parts of the heart than in the normal 
pace-making cells in the sino-auricular node. Distention of the 
ventricle may cause extra-systoles, the heart seeming to make an 
extra effort to empty itself. This may be due to very high arterial 
pressure or to feeblenees of the heart muscle, or, again, to obstruc- 
tion in the pulmonary artery distending the right ventricle. Extra- 
systoles usually cause jugular pulsation, which can be clearly seen. 

The diagnostic and prognostic importance of extra-systoles, 
which often cannot be felt at the wrist but can be heard or felt 
at the cardiac apex, depends entirely upon their cause. When 
met with in an otherwise perfectly normal individual particularly 
in healthy lads who lead an athletic life they have no significance 
other than increased cardiac irritability. Often moderate or 
severe exercise will temporarily dispel them. Such patients are 
perfectly good insurance "risks" and perfectly "fit" for exercise. 
If cardiovascular renal lesions are present, or if the patient 
suffers from some acute infectious disease, the proposition is 
completely reversed. 

When the rhythm is disturbed by the dropping of a beat the 
cause may be great fatigue of the ventricle as in some cases of 
very high blood-pressure or blocking of the contraction wave in 
His' bundle produced by overdoses of digitalis, disease, or func- 
tional disorder of these fibres caused by the toxemia of one of 
the acute infections. 

A dicrotic pulse is one which is characterized by a reduplication, 
which feels like a second beat following the first before the latter 
is over. It is found in many cases of exhausting fever, and depends 
upon an undue elasticity of the bloodvessels, with relaxation of the 
arterioles, so that the blood first unduly distends the arteries, which 
then contract upon it, and thus produce the second wave or apex 
to the pulse curve. 

We can study the pulse either by the touch or by the sphygmo- 
graph. If by the latter means, the instrument of Dudgeon is the 
best (Fig. 97) with which to take a single tracing. The normal 
pulse wave is shown in Fig. 98. 

It will be seen that there is a distinct upstroke produced, which is 
called the line of ascent. This is due to the distention of the artery 
produced by the ventricle forcing blood out into the aorta. There 
is after this a line of descent interrupted by two separate secondary 
waves, which are called catacrotic waves. The second or lower of 
these is called the dicrotic wave, and is the one which becomes 



282 



THE PULSE. BLOODVESSELS, AND BLOOD-PRESSURE 



marked enough to be felt in some cases of disease. The duration 
of the period of descent corresponds to the time the blood is flowing 
out of the arteries into the capillaries, and, if this flow is rendered 
difficult by vascular spasm or fibrosis, the line of descent will be 
gradual; if easy from vascular relaxation, it will be short. If the 




Fig. 97. — A sphygmograph. Certain supporting parts are omitted so that the 
multiplying levers may be displayed, a is a small metal plate which is kept 
pressed on the artery by the spring b. The vertical movements of a cause to- 
and-fro movements of the lever c about the fixed point d. These are communi- 
cated to and magnified by the lever e, which moves around the fixed point /. 
The free end of this lever carries a light steel marker which rests on a strip of 
smoked paper g. The paper is placed beneath two small wheels and rests on a 
roller which can be rotated by means of clock-work contained in the box h. The 
paper is thus caused to travel at a uniform rate. The screw graduated in ounces 
(Troy) is brought to bear on the spring b by means of a cam, and by this the 
pressure put on the artery can be regulated. The levers magnify the pulse 
movements fifty times. (Dudgeon.) 




Fig. 98. — a b, percussion upstroke, a b c, percussion wave, c d e, tidal wave. 
e f g, dicrotic wave, d ef, aortic notch, f g, diastolic period. 



drop is very sudden, it is a pulse of " empty arteries," so called, as 
after severe hemorrhage, in great feebleness, or in cases of aortic 
regurgitation. 

Very small irregularities of the line of descent are due to the 
elastic bloodvessels being thrown into vibrations by a forcible 
pulse wave. 



THE PULSE 



283 



In Fig. 99 is shown the typical pulse wave of aortic regurgita- 
tion; and in Fig. 100 that of mitral stenosis, which is irregular in 
time and volume. (See page 263.) 






Fig. 99. — A tracing taken from a case of aortic regurgitation. Corrigan's 
pulse. Note the sharp upstroke and the sudden fall. 



Fig. 100. — The small pulse of mitral stenosis. 

There still remains for consideration those states in which 
great arrhythmia or variation in pulse rate ensue as a result 
of incoordination between the auricles and the ventricles. Such 
a state may develop .as the result of the action of large doses 
of digitalis and also in mitral stenosis, in which disease it is 
very common. In mitral stenosis, or in any endocardial disease 
or myocardial degeneration which involves the fibres of His' 
auricular ventricular bundle, great cardiac irregularity develops 
if the bundle is partly destroyed, because only some of the con- 
tractile impulses which arise at the sino-auricular node reach the 
ventricle. If the entire bundle is destroyed we have a condition 
of complete heart-block, in which state the auricles beat very 
rapidly indeed, as can be determined by the jugular pulse, and the 
ventricles beat very slowly, originating their own impulses when 
deprived of the impulse arising in the sino-auricluar node because 
of the lesion. For reasons not well understood such a condition of 
complete heart block is often not constant but occurs in attacks. 
These attacks cause death or the patient presents a set of symp- 
toms called the Stokes-Adams syndrome. The general symptoms of 
this disease consist in a remarkably slow pulse, pulsation of the 
veins of the neck and sometimes attacks of vertigo, syncope, and 
apoplectiform or epileptiform seizures. (See Bradycardia.) 

Closely allied to the state just described is that form of con- 
stant arrhythmia in the pulse called by the various names of 
" absolute arrhythmia," "pulsus irregularis perpetuus," and "dis- 
orderly rhythm." The patient is, as a rule, weak and cyanotic, 
with distended jugular veins which may look as if the blood in 
them had a thrill. Not only is the pulse at the wrist irregular as 
to spacing of the beats, but the beats vary widely in size or force. 
A tracing of the jugular will show a single large ventricular wave 



284 



THE PULSE, BLOODVESSELS, AND BLOOD-PRESSURE 



at the time the ventricle contracts without the preliminary so- 
called a wave, due to normal auricular systole. Such a series of 




Fig. ioi. — Jacquet's sphygmocardiograph. 




Fig. 102. — Application of the sphygmocardiograph of Jacquet to a case of 
aneurysm with systolic retraction at the apex. The recording apparatus is 
bound on the wrist as is "the ordinary sphygmograph of Dudgeon. The radial 
pulse moves the lever nearest the arm, the jugular pulse is recorded by the lever 
attached by a tube to a tambour which is placed over the jugular vein and the 
apex beat by the lever nearest the wrist, which is connected by a tube to the 
tambour placed over the heart. 



symptoms is indicative of auricular fibrillation, a state of paralysis 
of the auricle in which this part of the heart fails to contract and 
acts solely as a dilated passageway for the blood to the ventricle. 



THE PULSE 



285 



The impulses passing from the sino-auricular node pass so rapidly 
over the auricle that the ventricle cannot respond, and sets up its 
own rate of beat. 



Shows the normal radial pulse on the lowest line, the apex beat on the middle 
line, the jugular pulse on the upper line. 



O/A^ 



Fig. 103. — Tracings taken with the Jacquet apparatus. 

A tracing from a case of "Stokes- Adams disease," which shows below the 
very slow pulse and in the middle the slow apex beat and above the rapid and 
abnormal jugular pulsation due to the regurgitation from the auricle, which 
is beating far oftener than the ventricle. 



For the purpose of getting a graphic record of these states of 
the circulation the instrument called the sphygmocardiograph of 



286 



THE PULSE, BLOODVESSELS, AND BLOOD-PRESSURE 



Jacquet may be used (Figs. 101 and 102). By means of columns 
of air in tubes the impulse of the jugular vein and the apex beat 
are recorded by levers as in Dudgeon's sphygmograph and a third 
lever by pressure from the radial artery produces a third tracing, 
each one being superimposed. (See chapter on the Thorax.) 




Fig. 104. — Simultaneous tracings of the apex beat, carotid, and radial pulse with 
Jacquet's cardiosphygmograph in a case of mitral stenosis. The apex and 
carotid show regular variations in groups of three. Two extra-systoles have 
occurred. The one at x is followed by a compensatory pause (intermission of the 
pulse) and an unusually forcible beat as the result of the prolonged rest period; 
the second at x' is immediately followed by the wave due to the normal sinus 
rhythm producing three beats in rapid succession (irregularity of the pulse), 
both the extra-systolic wave and that due to the normal sinus stimulus being 
small because of the short rest period which precedes each of them. The broad 
summit of the radiogram is indicative of a well -filled bloodvessel. 



BLOOD-PRESSURE IN HEALTH AND DISEASE. 

One of the most important acts of the physician is to make a 
skilful determination of the arterial pressure of his patient, since 
this is of even greater importance than the study of the pulse rate. 
Years of experience enable the physician to determine to some 
extent the tension of the arteries by his finger tips, and often the 
degree of tension gives him far more information than any other 
physical sign presented by the patient; but it is always best to 
employ a sphygmomanometer in order that an accurate observation 
may be made and a definite record in figures obtained. 

Before considering the variations from the normal in blood- 
pressure it must be recalled that in addition to the force expended 
by the heart in expelling blood from the left ventricle at each 
contraction the walls of the arterial system are provided with elastic 



BLOOD-PRESSURE IN HEALTH AND DISEASE 287 

tissue which yields to the impact of the cardiac systole and then 
contracts, urging on the blood. More important still, the blood- 
vessels are endowed with circular muscular fibres which are kept 
in a state of tonus by the vasomotor centre in the medulla and 
many subsidiary centres. The maintenance of this muscular 
tonus is essential to life, particularly in the smaller arteries or 
arterioles, as otherwise the blood in the arterial system would flow 
out into the great capillary networks, which are capable of holding 
several hundred times the volume of the blood in the arterial tree. 
By the force of the heart beat, the elasticity of the vessel walls, 
and the action of the muscular coats of the arterioles, the blood- 
pressure is varied according to the needs of the body, as under 
change of posture and under exercise. 

There is no fixed arterial pressure for every individual, a normal 
for every one at every age, as there is a fixed body temperature. 
Some persons have a higher or lower pressure than the average 
without indicating the presence of any abnormality. Men usually 
have a higher pressure than women, and the pressure of adults is 
always higher than that of children. The following figures give 
the approximately normal blood pressures at different ages: 

In infants, 60 diastolic to 80 systolic. 

In children, 70 diastolic to 90 systolic. 

In adolescents, 90 diastolic to no systolic. 

In young adults, 90 diastolic to 120 systolic. 

From thirty to fifty years, 90 diastolic to 130 systolic. 

From fifty to sixty years, 90 diastolic to 145 systolic. 

After sixty years, unless there is disease, the pressure usually 
falls 5 to 10 points. 

The Estimation of Arterial Tension. — Numerous investigators have 
devised apparatus capable of indicating the condition of arterial 
tension. The author will mention only those with which he has 
had large personal experience and satisfaction. One of the oldest 
and best for office use is Stanton's modification of the sphygmo- 
manometer of Riva-Rocci, which is well described in Fig. 105. 
The disadvantages of this apparatus are that it is easily broken, 
troublesome to carry about, because of its bulk, and, after a time, 
is apt to leak mercury or air. The principles of its use apply, 
however, to all mercurial sphygmomanometers. 

In applying the apparatus it is essential that the muscles of the 
arm shall be relaxed, and for this reason the limb should be sup- 
ported in an easy position. Usually it is best to have the patient 
seated or recumbent and to use the left arm as the manipulations 
by the physician are more easily carried out by the right hand. 

Before connecting with the manometer the latter should be placed 
on a firm, level surface and the mercury should stand at zero on the 
scale. This is readily accomplished by moving the scale up or down 



256 THE PULSE, BLOODVESSELS, AND BLOOD-PRESSURE 

on the glass tube. The connection having been made, the valve B 
is screwed tight and the valve A opened (arm parallel to the 
horizontal arm of the T). With the finger of the left hand on 
the pulse the right hand works the pump. Compression of the 
bulb forces air into the closed system — distending the rubber 




Fig. 105. — The systolic pressure is determined by noting the point at which the 
pulse reappears at the wrist after obliteration, while the diastolic pressure may be 
estimated by recording the point at which the greatest oscillations occur in the 
mercury column of the manometer. The pressure is applied to the arm by a rubber 
armlet, which is 10 cm. wide. This armlet is prevented from expanding outward 
by a cuff F of double thick canvass with inserted strips of tin, which is held in 
place by two straps, which completely encircle the cuff. On the rigidity of this 
depends, to a large extent, the transmission of pulsation. The rubber armlet is 
connected with a stiff -walled rubber tube G, which in turn connects with the 
manometer. The chamber C communicates by means of a metal tube with the 
glass column D, which is connected by a screw thread at 3, the caliber of C being 
approximately 100 times that of D. The cap of the chamber which screws on is 
provided with a metal T, which is connected at 2 with the rubber armlet and at 
1 with the bulb used as an air pump. At A is a stopcock shutting the rubber 
bulb completely from the rest of the apparatus, while at B is a screw valve which 
allows the air to escape from the closed system. When desired this manometer 
can be made portable (without removing the mercury) by screwing the caps 
1 and 2 into either end of the T at 1 and 2. Then tilt the manometer away from 
the glass column D until all the mercury has run into the chamber; unscrew the 
glass and screw in cap 3. Before removing cap 3 the manometer must always be 
tilted, else the mercury will be lost. Pressure is established in the apparatus by a 
double bulb syringe similar to those used with the thermocautery. 

armlet and with the same degree of force, displacing the mercury 
in C, driving it up the glass column D. When the pulse is no 
longer felt, the arm of the valve A is turned until it is at right 
angles with the thumb and finger. The valve B is now slowly 
unscrewed until the mercury column begins to fall. With the 
eye on the scale, the point at which the pulse reappears is mentally 



BLOOD-PRESSURE IN HEALTH AND DISEASE 289 

noted as the systolic pressure. Any pulsation noted in the mercury 
column before the pulse beat reappears at the wrist is to be dis- 
regarded. As the mercury column falls the oscillations in the 
mercury increase in size until they reach a maximum and then 
decrease. The base line of the greatest oscillation (the line from 
which it starts) is the diastolic pressure. 

A much more accurate method of estimating the systolic and 
diastolic pressure is by the auscultation of the brachial artery 
by a small phonendoscope at the same time that the eye watches 
the mercury column (KorotkofPs method). The compression of 
the arm by the cuff having been induced to such a point that 
the pulse is lost at the wrist, the air is allowed to slowly escape. 
At the same instant that the radial pulse returns a distinct tapping 
sound is heard in the brachial artery (phase i), and this repre- 
sents systolic pressure as seen on the gauge. The tapping or 
arterial sound becomes more like a murmur (phase 2), and if the air 
is allowed to escape very slowly, the sound becomes less murmurish 
and sharper (phase 3). It then fades away (phase 4), and finally 
ceases. Just as it begins to fade away, reading the scale on the 
sphygmomanometer will give the diastolic pressure. It is worthy 
of note that in aortic regurgitation the tapping sound in the 
brachial artery lasts until the mercury column has fallen to zero. 
The systolic pressure can be well estimated by the finger on the 
artery, but the auscultatory method is the only accurate means 
of getting the diastolic pressure. 

The sum of the systolic pressure and the diastolic pressure in 
millimeters of Hg divided by 2 gives us the mean pressure which 
in turn informs us of the general circulatory state. The diastolic 
pressure is the blood-pressure without the impulse of the ventricular 
contraction and, therefore, if we subtract the diastolic pressure from 
the systolic pressure the difference represents the force of the heart's 
contraction or systole. 

In nearly all cases the first estimation will be found 10 to 20 mm. 
higher than subsequent estimations. This is probably due to 
excitement arising from fear that the examination will cause pain. 
Several estimations should be made until the level normal for the 
individual is obtained. Often it is best to have the patient rest 
in bed for some hours before the test is made. 

The Nicholson pocket sphygmomanometer is as accurate as 
the Stanton apparatus just described, is very portable, small in 
bulk, and not easily broken or gotten out of order if ordinary 
care is exercised. By using a glass tube which is large in caliber 
separation of the mercurial column when the instrument is carried 
about is prevented. By having a folding and movable metal scale 
and a glass tube which can be separated into two parts it is possible 
to enclose this instrument in a very small space. (See Fig. 106.) 
19 



290 



THE PULSE, BLOODVESSELS, AND BLOOD-PRESSURE 



It is provided with a very convenient cuff which, when put 
around the arm, is fixed in place by having its end tucked in, so 
avoiding the use of straps or buckles, and which fits the arm very 
snugly. The author has found this a great improvement over 
the more old-fashioned instrument already described, both as to 
the mechanism of the apparatus and the form of the cuff. 




Fig. 106. — The Nicholson pocket sphygmomanometer set up for use. The 
cuff is seen about the upper and middle third of the arm. The air pressure in 
the cuff and on the mercury is produced by the small pump in the operator's left 
hand. The right hand holds a binaural stethoscope over the brachial artery 
in order that the systolic and diastolic pressure may be estimated by the auscul- 
tatory method of KorotkofT. The upper half of the glass tube fits into the 
lower half by a ground-glass joint. The mercury cannot escape because of 
the other valves shown by the handles. 

Another excellent mercurial instrument easily carried and not 
easily broken or disordered is the Mercer (Fig. 107). If the 
mercury separates in the tube it can be easily shaken down by 
the same movement that is used in shaking down the mercury 
in a clinical thermometer. The scale can readily be adjusted to 
the height of the mercury if there is any variation. The armlet, 
or cuff supplied, is not as handy as the soft armlet just described, 
as it is applied with buckles. The air is forced by an ordinary 
bulb with a by-pass attachment whereby pressure can be varied. 



BLOOD-PRESSURE IN HEALTH AND DISEASE 



291 



This apparatus is sufficiently accurate for all purposes, and 
possesses the great advantage of cheapness. 




Fig. 107.- — -The Mercer sphygmomanometer. 

The so-called Tycos sphygmomanometer (Fig. 108) is not a 
mercurial instrument, but is constructed of metallic spring tam- 
bours, by means of which an indicator revolves on a dial and so 
indicates the pressure in the cuff, which is of the soft, easily applied 
type already described. This is an excellent instrument because 
its very small size renders it easy to carry and because the indi- 
cator hangs on the cuff where it is readily seen by the physician, 
and where it cannot be seen by the patient. This permits its 
use without a table or assistant to hold the apparatus and renders 
it easy of application when a patient is in bed. My experience 
has been that these instruments are sufficiently accurate for all 
purposes if carefully taken care of. Any doubt as to their accuracy 
can be at once settled by coupling the cuff to a mercurial instru- 
ment, which is, of course, the standard, if the surface of the mercury 
and the zero of the scale are on a level at the start. 

Temporary High Tension. — Taking up first high tension we find 
that we can consider it as normal and pathological. The normal 
cases are those in which the tension is raised by exercise or excite- 
ment, such tension being a natural or physiological response. This 
form of high tension possesses no interest for the clinician unless it 
is associated with the presence of a weak heart or is so great and 



292 



THE PULSE, BLOODVESSELS, AND BLOOD-PRESSURE 



prolonged that it produces cardiac distress or injury. It is, however, 
the form of high tension that frequently damages the heart of the 
sedentary and elderly man who suddenly decides that he needs exer- 
cise and takes it to a strenuous and excessive degree. Another type 
of normal high tension, in one sense of the word, is met with in the 
stage of onset of acute febrile diseases when it may be an effort on 
the part of the body to supply more blood to certain areas for 
protective purposes, for all large capillary net-works are poison 
destroyers. Still another normal or beneficial type of high tension 
is the high tension of intracranial injury or disease, in which states 




Fig. 108. — The Tycos sphygmomanometer. 

Cushing has shown us that the rise is essential to the preserva- 
tion of life. If Cushing is right, how many persons have been hur- 
ried to their end by bleeding in apoplexy. In early CO poisoning 
the rise of tension is designed to send more blood to the respiratory 
centre, and the rise due to severe pain, as in renal colic, lead colic, 
and labor, may all be advantageous. In the latter case (labor) I 
have elsewhere pointed out that it is this rise of tension produced 
by pain that permits women in labor to take chloroform with rela- 
tive impunity. These facts should make us cautious in the use of 
vascular relaxants, unless we are certain that the high tension is 
useless and actually harmful. 



BLOOD-PRESSURE IN HEALTH AND DISEASE 293 

An abnormally high pressure in a patient entering upon an 
attack of pneumonia is of considerable significance, since this 
means not only that the heart is subjected to an additional strain, 
but also points to the strong probability that an underlying insidi- 
ous nephritis or cardiovascular-renal fibrosis is present. 

If, during pregnancy, a state occurring during the early decades 
of adult life when arterial changes are very rare, it is found that 
the systolic blood-pressure is as high as 160, this is an important 
sign of approaching eclampsia and if the pressure is above even 
130 the urine should be carefully examined and the patient kept 
under treatment and observation. 

Persistent High Tension. — A high blood-pressure constantly 
maintained is practically always associated with either spasm of 
the arterioles or arteriocapillary fibrosis, or both, and with a 
more or less well-developed chronic contracted kidney and cardiac 
hypertrophy. The state of chronic contracted kidney, or inter- 
stitial nephritis, is the cause, or at least the accompaniment, of the 
arterial state, but the cardiac condition is secondary to the vascular 
and renal changes, except in those cases in which the fibroid 
process involves the heart early in the disease. An examina- 
tion of the urine in such cases will often reveal the low specific 
gravity, the trace of albumin and the hyaline casts of chronic 
contracted kidney. Sometimes, however, the high blood-pressure 
is due to chronic parenchymatous nephritis, but in such a case 
the picture of disease presented by the patient is quite different. 

A constant abnormally high tension is, however, not always evil 
by any means. High tension is actually needed to drive blood 
through fibroid vessels to distant parts for their proper nutrition. 
The heart in many cases of high tension has undergone compensa- 
tory hypertrophy, and this increased power and the high tension 
help to feed the heart muscle itself through the coronary vessels 
and the vessels of Thebesius. Very often the vascular system in 
high tension may be considered to have established for itself a 
new standard of pressure, say of 170 to 180, and if this is reduced 
a state is developed which may be considered as abnormal, as is a 
pressure below the true normal in an ordinary individual. In other 
words, in studying high pressure, it is not sufficient to study the 
pressure alone. We must study the whole cardiovascular apparatus. 

Brunton has recently advanced the view that not only does 
high arterial tension do harm by interfering with the nutrition 
of the tissues, but also by interfering with the nutrition of the 
vessels themselves. Thus he points out that the high tension 
compresses the vasovasorum between the inner coats and the 
fibrous coat, which is fixed, because it has reached the point of 
fixation by distention. Again, he advances the view that the 
normal constant expansion and contraction of vessels in health, like 
massage, maintains and aids the blood flow in the vasovasorum. 



294 THE PULSE, BLOODVESSELS, AND BLOOD-PRESSURE 

What is the significance of high tension as to the heart? If its 
sounds are approximately normal we learn that it is still a fairly 
healthy organ, able to stand up to its work, but we must bear in 
mind that in many men past middle life a state of increased tension 
exists which is not appreciated because the heart has gradually 
become accustomed to the strain. The stress and strength are so 
nearly balanced that when a sudden increase in exertion is made, as 
in running for a car, or taking any form of violent exercise, cardiac 
dilatation due to overstrain at once develops. Abnormal increase 
in tension means increased work for the heart muscle and increased 
strain upon its valves, particularly the aortic and mitral leaflets. 
The result of this strain is speedily manifested in a previously 
normal heart by hypertrophy with associated dilatation, in a 
previously feeble or diseased heart by dilatation with increase in 
its feebleness, in failure of the mitral valves to stand the great 
pressure brought to bear on them with each systole, a failure 
increased in effect by the fact that the mitral ring is feeble also, so 
that mitral regurgitation takes place, the result being that the 
blood finds it as easy to slip back into the auricle as to pass out 
into the aorta. In some instances this leak at the mitral orifice is 
advantageous for a time because it acts as a safety valve and 
relieves the ventricle of excessive strain. The high tension due 
to narrowing of the arterioles is not alone responsible for cardiac 
distress; for the very fixation of the vessels increases the work of 
the heart, and with fixation comes unyielding tortuosity, which 
demands increased cardiac effort. The heart now fails not alone 
from overwork, but in addition it may begin to develop degener- 
ative changes in its fibres, for the same factors that act deleteri- 
ously on the muscular fibre of the vessel wall also act on the more 
specialized muscular fibres of this organ and its own blood supply 
fails because the coronary arteries are in spasm or fibrosis. 

A useful test to reveal the reserve force and ability of the heart 
consists in taking the blood-pressure while the patient is at rest 
and then, after he has climbed a flight of stairs, to take it again 
at once. If the patient's heart has reserve energy the blood-pres- 
sure after the exertion should be raised 5 to 15 millimeters, but if 
the heart is impaired in strength the pressure not only does not 
change but falls in direct proportion to the cardiac feebleness 
and the severity of the exercise, because the heart has not the 
power to meet the increased circulatory demand. 

If the blood-pressure be taken in the arm of a patient who has 
aortic regurgitation it is always high, usually about 160, and in 
the leg 40 to 100 millimeters higher than in the arm (200-260). 
The patient must, of course, be lying prone when the test is made, 
so as to avoid the difference due to hydrostatic pressure if he were 
erect. In a prone patient such a difference is pathognomonic of 
aortic regurgitation. 



BLOOD-PRESSURE IN HEALTH AND DISEASE 



295 



Low Tension. — Having considered some of the facts which con- 
cern hypertension in the arterial system, we have still before us the 
study of hypotension. Such a condition is rare as compared to 
hypertension, and is most frequently met with as a part of some 
suddenly developed condition in the course of an acute illness, or 
as a result of accident or surgical shock. 



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100 

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120 
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Fig. 109. — Case of croupous pneumonia. Blood-pressure normal and well 
separated from pulse rate. No treatment by stimulants needed. Third line from 
bottom of chart represents blood-pressure. 



If a patient suffering from croupous pneumonia has a blood- 
pressure expressed in millimeters of mercury approximately the 
same as his pulse rate per minute, he may be considered as danger- 
ously ill. If his pressure is the same as or less than his pulse 
rate he will probably die unless active treatment can alter the 



296 



THE PULSE, BLOODVESSELS, AND BLOOD-PRESSURE 



ratio for the better. If, on the other hand, his pulse rate is much 
less than his blood-pressure so expressed, he is in no immediate 
danger. Thus if the blood-pressure is 130 and the pulse 90, there 
is a difference of 40 points between his blood-pressure and his 
pulse rate, and he is doing well (Fig. 109), whereas if the pressure 
is 100 and the pulse rate no he is in very great danger (Fig. 
no). If, under active treatment the pressure rises to no and the 
pulse drops back to 100, a distinct improvement is known to have 
taken place. This test loses its value largely or completely in the 
following classes of cases: 




Fig. 1 10. — Case of croupous pneumonia in which the near approximation of 
blood-pressure and pulse rate required active stimulation, thereby saving life. 
With the occurrence of crisis the pulse rate and the blood-pressure assumed a 
normal relationship. Third line from bottom of chart represents blood-pressure. 



In old people who have hypotension, as a result of their age 
and feebleness, before they are taken ill. Such cases also often 
fail to present that other triad of croupous pneumonia, namely, 
the slow pulse, rapid respiration, and high temperature. 

The second class in which it fails is in children in whom the 
blood-pressure is naturally low, so that the pressure and the 
pulse rate are normally nearer together than in adults. 



BLOOD-PRESSURE IN HEALTH AND DISEASE 297 

The third class is in stout, flabby women who may be said to 
present some of the signs of a mild hypothyroidism. 

The fourth class is represented by those cases in which the 
pneumonia is a sequence or complication of a severe illness like 
typhoid fever. 

The fifth class is represented by pneumonia complicating 
diabetes. 

In all of these cases the relative slowness of the pulse rate as 
compared to respiratory rate in pneumonia is also usually lacking. 

In catarrhal pneumonia, in which the relative disproportion of 
pulse rate and respiration seen in croupous pneumonia is absent, 
the sign is of little value, unless the catarrhal pneumonia occurs 
in a case of hypertension arising from a previously existing vascular 
spasm or arteriocapillary fibrosis, when it is of value. 

When the hypotension is chronic it depends, in the great 
majority of instances, upon feebleness of the heart muscle, but in 
one particular malady at least we have a persistent low tension 
not so much as a result of cardiac feebleness as of vascular relax- 
ation, namely, exophthalmic goitre, in which disease the thyroid 
secretion acts as a powerful vascular sedative. The blood-pressure 
is also remarkably low in Addison's disease. 

Not rarely in neurasthenic persons, or persons who are suffering 
from the after-effects of an acute illness, hypotension is an im- 
portant factor. Thus, persistent diurnal somnolence may exist 
while the patient is up and about, replaced by marked nocturnal 
wakefulness as soon as he lies down. This state is due to a low 
tension which prevents an adequate supply of blood to the brain, 
which organ immediately becomes active as soon as the recumbent 
posture is assumed. 

Suddenly developed hypotension in the later stages of acute illness 
may be considered under two headings : The first type is met with at 
the critical period of acute infections, of which the most noteworthy 
is, perhaps, croupous pneumonia. It is not uncommon to find in 
these patients at this time a state bordering on collapse: the face is 
anxious, the forehead, wrists, and the trunk bedewed with sweat, 
the pulse very full, but the arteries relaxed, and the heart's action 
excessive, as it actively endeavors to fill the leaking vessels, which 
do not offer the normal resistance to its action. This state depends 
chiefly, if not entirely, upon vascular hypotonus. The second 
type is met with in the course of prolonged fevers, such as typhoid 
fever, in which the vessels relax partly from toxemia producing 
degenerative changes in the vessels and partly from lowered 
nervous force. 



CHAPTER X. 
THE ABDOMEN AND THE ABDOMINAL VISCERA. 

The surface of the abdomen — Changes in the appearance and shape of the 
abdominal wall — The signs and symptoms of disease of the abdominal 
organs. 

The condition of the abdominal surface and abdominal contents 
is best studied by means of inspection, palpation, percussion, and 




HIGHEST LEVEL 
OF ILIAC CREST 



Fig. i io. 



-The regions of the abdomen and their contents, 
cartilages in curved outline. (Gray.) 



Edge of costal 



auscultation. For the purposes of inspection the surface of the 
abdomen has been arbitrarily divided by diagnosticians into a 
number of spaces, which are best shown in Fig. no, and which 



INSPECTION 



299 



get their names from the regions in which they are located, or 
from the organ immediately underneath the abdominal wall. By 
means of these arbitrary outlines we can readily describe the 
exact spot in which a physical sign or symptom is found. 1 

The following table, from Gray's Anatomy, clearly shows the 
viscera to be found under each of the areas named : 



Bight Hypochondriac. 
The right lohe of the liver 
and the gall-bladder, hepatic 
flexure of the colon, and part 
of the right kidney. 



Eight Lumbar. 
Ascending colon, part of the 
right kidney, and some con- 
volutions of the small intes- 
tine. 



Right Inguinal {Iliac). 
The caecum, appendix cseci. 



Epigastric Region. 
The pyloric end of the 
stomach, left lobe of the liver, 
and lobulus Spigelii. the pan- 
creas, the duodenum, parts of 
the kidneys and the supra- 
renal capsules. 

Umbilical Region. 
The transverse colon, part of 
the great omentum and mes- 
entery, transverse part of the 
duodenum, and some convo- 
lutions of the jejunum and 
ileum, part of both kidneys. 

Hypogastric Region. 
Convolutions of the small 
intestine, the bladder in chil- 
dren, and in adults if dis- 
tended, and the uterus during 
pregnancy. 



Ltft Hypochondriac. 
The splenic end of the stom- 
ach, the spleen and extremity 
of the pancreas, the splenic 
flexure of the colon, and part 
of the left kidney. 

Left Lumbar. 
Descending colon, part of the 
omentum, part of the left kid- 
ney, and some convolutions of 
the small intestine. 



Left Inguinal (Iliac). 
Sigmoid flexure of the colon. 



Inspection.- — On inspecting the abdominal surface the physician 
should look for eruptions which may indicate some general disease, 
as typhoid fever; for localized swelling, which may be due to hernia; 
for strise, indicating that the skin has been stretched by excessive 
fat, by great swelling from ascites, or by pregnancy. He should 
also in a case of suspected early pregnancy look for a dark streak 
in the median line. If the umbilicus is protruding and tense it 
may indicate distention due to grave abdominal disease, or it may 
be infiltrated by a morbid growth which has been primarily hepatic. 
If it be a secondary growth the navel will perhaps be " moored 
fast." Sometimes it is much swollen from chafing and eczema. 
Umbilical hernia may be found. 

The general abdominal wall is protruded and retracted in normal 
respiration in both sexes, but more markedly so in males. It is 
pushed outward, or protruded, by many perfectly normal causes, 
such as an unusual amount of fat in the omentum, pregnancy, and 
an accumulation of liquid and food in the stomach after a heavy 
meal. It is also convex to an abnormal degree in cases in which 
ascites is present, when the stomach and bowels are overdistended 
with gas (tympanites), and when any of the organs found in the 



1 For changes in the skin of the abdomen, see chapter on the Skin. 



300 THE ABDOMEN AND THE ABDOMINAL VISCERA 

abdominal cavity are the seat of swelling or tumors of large size. 
In children a protruding pot-belly, "the frog-belly," of the French, 
is seen in cases of scrofula or tuberculosis of the mesenteric glands, 
and in those cases which suffer from chronic gastro-intestinal 
catarrh or a dilated stomach or colon. 

If the belly wall is retracted, concave, or " scaphoid," as it is 
sometimes called, we look for the cause in abstinence from food, or 
remember the possibility that excessive vomiting or purging may 
have emptied the gastro-intestinal tract of its usual contents. We 
also find a retracted belly wall in nearly all cases of advanced 
wasting diseases, such as carcinoma, peritoneal tuberculosis of the 
cirrhotic type, or tuberculosis of the lungs; with wasting; and if the 
retraction is associated with muscular rigidity of the belly wall and 
pain, we suspect the early stages of peritonitis or the presence of 
some acutely painful affection, such as renal or hepatic colic or 
lead colic. Marked concavity and retraction of the belly wall are 
also seen sometimes in cases of tuberculous meningitis. 

Sometimes in thin patients with some atrophy of the abdominal 
muscles or in cases of diastasis peristaltic waves are to be seen 
traversing the abdominal surface as the result of violent movements 
of the bowels. These waves are commonly seen in cases of intes- 
tinal obstruction, and in neurotic persons with mucomembranous 
enteritis, or, if in the epigastrium, they may be due to a dilated 
stomach. If the waves are from below upward and in the right side, 
they are probably arising in the ascending colon; if from above 
downward and in the left side, in the descending colon and sigmoid 
flexure. Again, gastric waves pass from left to right, while those 
in the transverse colon pass from right to left. 

Distention of the Abdominal Wall. — The abdomen is distended 
very greatly by gas in many cases of peritonitis, typhoid fever, 
and in persons suffering from flatulent colic. If this be the cause 
of the distention, percussion of the anterior and lateral belly wall 
when the patient is lying on the back will give a tympanitic note. 
We separate, diagnostically, the swollen abdomen due to wind 
from that due to ascites by the fact that in the latter condition 
the epigastrium is moderately flat when the patient is lying down, 
while when tympanites is present it is more protruding. Again, in 
ascites the greatest bulging is generally to be found in the flanks, 
or, if the patient sits or stands erect, the hypogastric region bulges 
from the change in the position of the fluid. If the swelling be 
due to a moderate-sized ovarian cyst, this variation in form will 
not occur, as the cyst is not readily movable. If the ovarian 
tumor be large, the differential diagnosis may be most difficult 
and almost impossible, except by the history or by examining the 
liquid withdrawn by tapping, which is a dangerous procedure if 
the cyst proves to be papillomatous. 



DISTENTION OF THE ABDOMINAL WALL 



301 




Fig. hi. — Enormous ascites. The area inside the line is that which was 
resonant on percussion (gut tympany). On either side and below the line there 
was absolute flatness due to the presence of fluid. (From the author's wards.) 




Fig. 112. — Same as Fig. 105. When the patient was turned on the side the 
fluid flowed in that direction, and so the area of resonance was altered, the area 
of flatness on the right increasing and on the left diminishing. 



302 



THE ABDOMEN AND THE ABDOMINAL VISCERA 



In cases of ascites due to free liquid in the abdominal cavity per- 
cussion will elicit flatness over the flanks and resonance where the 
intestines containing gas are floated up against the anterior belly 
wall above the effusion. Sometimes, however, if the large intestine 
be empty of fecal matter, percussion in the flank behind the mid- 
axillary line will reveal tympany, because the peritoneum walls 
off the liquid from the posterior surface of the bowel. If the patient 
is turned slightly to one side, the area of flatness on percussion is 
altered, as is shown in Fig. 112. Palpation will also reveal fluctua- 




Fig. 113. — Showing method of determining the presence of fluid in abdomen 
by transmitted fluctuation. The hand of an assistant is placed on the edge on 
the middle line, to prevent transmission of impulse by the belly wall. The right 
hand then naps the flank, and if fluid is present the impulse is felt by the left 
hand on the other side. 



tion in ascites, but none in tympanitic distention. To develop this 
fluctuation, the patient is placed on his back and the finger, tips 
of the left hand of the physician are placed against the skin of the 
flank. With the finger tips of the right hand the opposite flank 
of the patient is struck a blow as in performing ordinary per- 
cussion, when the impulse, if fluid is present, will be transmitted 
to the fingers of the left hand. To prevent a transmission of the 
impulse through the abdominal wall, an assistant may press with 
the edge of his hand over the linea alba (Fig. 113). Increasing 



PLATE TX 




Median Vertical Section of Body of a Boy of Seventeen, who Died of Colloid 
Cancer of the Peritoneum and lliae Flexure. 

The gelatinous masses represent the growth and the ascitic fluid is readily seen. (Ponfick's Atlas.) 



DISTENTION OF THE ABDOMINAL WALL . 303 

intra-abdominal pressure causes the floating ribs to become pushed 
outward, the apex beat of the heart is often displaced upward 
and outward, and the umbilicus becomes protruded instead of 
retracted. The skin of the belly wall becomes thin and shining, 
and the recti muscles may become separated. After tapping in 
such cases the peristaltic movements of the bowels can be readily 
felt through the intervening skin. 

Having decided that the distention is due to an accumulation of 
free fluid in the abdomen, it remains for the physician to determine 
what the cause of the ascites may be. Its most frequent cause is 
atrophic cirrhosis of the liver, which results in engorgement of the 
abdominal vessels with secondary transudation of fluid. (See Fig. 
121). If it be not due to cirrhosis, it may arise from an abdominal 
tumor, which by pressing on large vessels results in an effusion of 
liquid through their walls, or be caused by tuberculous peri- 
tonitis, by obstruction of the thoracic duct, by valvular diseases 
of the heart causing an obstruction to the flow of blood in the 
vena cava, or, finally, by chronic parenchymatous nephritis. If 
the last causes be present, there will be some edema of the lower 
extremities or general anemia with dyspnea and albuminuria. 

Very often in cases of ascites, particularly when this condition 
arises from hepatic cirrhosis, there is developed on the anterior 
belly wall a more or less well-defined bunch of veins, which is some- 
times called the caput Medusa, as the result of an attempt at 
collateral circulation, to compensate for the obstructed flow caused 
by the changes in the liver. Sometimes a mediastinal growth will 
cause a somewhat similar development. When the obstruction is 
lower than the liver the superficial veins of the lower part of the 
abdomen (hypogastrium) will be found distended. 

Localized bulging of the abdominal wall, chiefly on the right 
side, is found in cases in which the liver is enlarged by hypertrophic 
cirrhosis, or by cancer or other morbid growth, such as gumma or 
sarcoma, and by abscess. The swelling, if its origin be in the liver, 
will arise under the floating ribs on the right side, and will extend 
downward and forward toward the umbilical area. If the enlarge- 
ment be great, it will extend far below the umbilicus and across 
the umbilical area to the opposite side of the abdomen. 

In enlargement of the spleen, similar signs, springing from the 
floating ribs well over to the left side, may be developed (see Figs. 
118 and 125), and a large cystic kidney on either side may cause 
abdominal bulging, particularly if the kidney be floating. (See 
Floating Kidney and Spleen.) 

Marked swelling of the epigastrium indicates distention of the 
stomach by gas or food, or that this organ is the seat of morbid 
growth. Sometimes a similar distention results from enlargement 
of the posterior mediastinal and retroperitoneal glands. Again. 



3°4 



THE ABDOMEN AND THE ABDOMINAL VISCERA 



distention of the epigastrium is apt to be caused by enlargement of 
the left lobe of the liver. This is an important point to remember 
in abdominal diagnosis. 

Cases of dilatation of the stomach often show very great bulging 
of the epigastric umbilical area when that viscus is distended by 
liquid and gas. 

In ovarian tumors the growth often gradually distends the entire 
belly equally; but as already stated, the history is usually that of 
swelling, low down, and of its being chiefly unilateral at first. 







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Fig. 114. — Outline of normal position and size of an adult stomach when 
distended with gas. 

It should be remembered that the discovery of a pyriform swelling 
in the hypogastrium may possibly be due to a pregnant uterus, 
or to retention of urine, with consequent distention of the bladder. 

Gastric Dilatation.— Gastric dilatation results from obstruction 
of the pylorus or from inherent feebleness of the stomach wall, and 



GASTRIC DILATATION 



305 



when it is present the entire upper part of the abdomen may be 
found distended, and tense but yielding. The history will show 
that the patient is attacked now and again by vomiting, during 
which a most extraordinary quantity of food and liquid, which has 
gradually accumulated, will be expelled. 




Fig. 115. — Showing diagrammatically the change in the position of the 
stomach in dilatation, and how difficult it is for this organ to empty itself 
of fluids. 



We discover the condition of the stomach as to its size and shape 
by means of washing it clean with the stomach tube and then filling 
it with a known quantity of water, which can be siphoned out and 
measured. Or instead we first wash out the stomach by means of a 
stomach tube and then fill it with gas by giving the patient to drink, 
first, a half-glass of water with 1 dram of sodium bicarbonate in it, 
and then another half-glass with 30 gr. of tartaric acid dissolved in 
it, so that gas will distend the viscus. One is able with ease in a thin 
20 



306 



THE ABDOMEN AND THE ABDOMINAL VISCERA 



person, by means of percussion, to outline the stomach by the area 
in which a high-pitched tympanitic note is heard. It is best to 
mark the edge of gastric resonance by means of a blue pencil, and 
thus map out the gastric area. Instead of this, we may distend 
the stomach with air by attaching a Davidson syringe to a stomach 
tube or by using an atomizer bulb. 




Fig. 116. — Gastroptosis and enteroptosis due to relaxation and atrophy of 
belly wall. Hornet's nest belly. 



Even before the stomach is artificially distended with gas, per- 
cussion may give us valuable information, for if obstruction of the 
pylorus exists, there may be found either a large area of gastric 
tympany through the accumulation of gas from fermentation, or, 
if no vomiting has taken place for some time, an equally great 
area of gastric dulness due to an accumulation of food and liquid. 
Fig. 114 shows the normal gastric area when the stomach is dis- 
tended with gas. 

Another very valuable method of determining the presence of 
gastric dilatation and gastroptosis is by the employment of the 
x-ray and large doses of bismuth, which substance is used because 
it is opaque. The dose of bismuth subcarbonate must be massive. 



PLATE X 




X-Ray Picture of Gastroptosis. The Viseus is well down in the Pelvis and 

well filled with Bismuth. 



GASTRIC DILATATION 307 

as much as i or 2 oz. held in suspension in a pint of kefir. The best 
results are naturally obtained when the patient is in the erect 
position. Either the fluoroscope or the radiographic plate may be 
employed. Usually it is best to use both methods. 

In addition to the dilatation revealed by the x-ray and bismuth, 
it will be found that the stomach empties itself of the bismuth 
meal with great slowness, the bismuth often remaining for from six 
to twelve hours or more. Sometimes, too, the x-rays show that the 
pyloric region is thickened and enlarged, thus revealing the presence 
of hypertrophy or morbid growth which obstructs this orifice. 

In some cases symptoms of gastric dilatation may arise from the 
presence of " hour-glass stomach" a state in which a stricture divides 
this organ more or less completely into two or more parts. (See 
Fig. 117.) The presence of this state may be determined by rilling 
the stomach with water and gas from the halves of a Seidlitz powder 
taken separately. On percussion it will be found that the cardiac 
area is distended but the pyloric area is empty, and some minutes 
later the pyloric portion becomes distended. During this period the 
use of a stethoscope over the middle area of the stomach may 
reveal the sounds made by the passing of the fluid or gas through 
the stricture. If the stomach is washed out by lavage until the 
liquid is clear and then after a short time washed again and the 
returned liquid is found to be foul, this is a sign of hour-glass 
stomach, because the cardiac area has been filled by retained 
contents on the pyloric side of the stricture. By far the best 
method, however, is to use a bismuth meal and the x-ray. 

When the hypogastric area is very protuberant, and after a dis- 
tended bladder or a pregnant uterus has been excluded, the cause 
may be considered, in women who have borne several children, as 
enteroptosis. The abdominal wall having atrophied fails to hold 
the abdominal contents at their proper level. Enteroptosis also 
occurs in men and women who have lost much fat and in those who 
have a defective carriage so that the abdominal contents are not 
properly supported. (See Fig. 116.) 

In many cases of enteroptosis, the use of "Glenard's belt sign" 
may be resorted to. This consists in standing behind the patient, 
placing the hands upon the lower part of the abdomen and lifting 
upward and backward, when if gastroptosis or enteroptosis is 
present relief from the sense of dragging may be felt. 

I have found this method of diagnosis very serviceable. 

In inspecting abdominal swellings the physician should watch to 
see if they move up and down with respiration. If they do, they 
are probably connected with the diaphragm and depend upon 
disease of the liver and spleen, as tumors of the pancreas, stomach, 
and kidney are usually not attached to the diaphragm, and there- 
fore generally do not move. 



3 o8 



THE ABDOMEN AND THE ABDOMINAL VISCERA 



Inspection of the abdominal wall will also show possible venereal 
infection if the glands in the groin are enlarged, or if in suppurating 
they have left puckered scars. 




Fig. 117. — Hour-glass stomach. 




Fig. 118. — A case of splenic anemia with great enlargement of the spleen, as 
shown in the large outlined, area. The smaller outlines indicate the areas of 
anemic murmurs near the base of the heart and in the carotid artery. (From 
the author's wards in the Jefferson Medical College Hospital.) 



PALPATION AND PERCUSSION 309 

Palpation and Percussion. — More important than any other 
external method of studying the condition of the abdominal con- 
tents is the use of gentle palpation, the fingers being gradually 
worked down into the abdominal cavity in such a way as not to 
cause pain or excite the muscles of the abdominal wall to resistance. 
The hand should always be carefully warmed before palpation is 
attempted. The object of the examiner is to discover, first, the 
hardness or resistance to pressure; secondly, the consistency and 
form of the organs which he can touch; and, thirdly, whether any 
swellings which he feels are movable, bound down and immovable, 
pulsating, soft or hard, nodular or smooth. The patient whose 
abdomen is to be palpated must be placed flat on his back, with 
the knees drawn up to relax the abdominal muscles; the head and 
neck should be raised, and, if possible, the attention of the patient 
should be diverted by conversation about some symptom which 
exists elsewhere than in the belly, while the examination is made, 
as in this way voluntary muscular resistance is removed to some 
extent. He should be made to breathe easily through his opened 
mouth; and if the belly wall remains so rigid that a perfect exami- 
nation is impossible, and yet the results of such an examination are 
very important, ether or chloroform should be given to relax the 
muscles. In other instances in which it seems inadvisable to give 
an anesthetic, the patient may be examined in a bath as hot as he 
can bear. He should be entirely submerged up to the neck. The 
hot bath often relaxes the abdominal wall sufficiently to aid diag- 
nosis very greatly. 

After the abdominal contents have been carefully examined, the 
patient being on his back, he should be placed first upon one side 
and then upon the other, and the abdominal contents again pal- 
pated. This is particularly necessary when examining the belly 
for growths or when enlargement or displacement of the liver, 
spleen, or kidneys is suspected. 

It must be remembered, however, that the anterior abdominal 
wall, particularly that of nervous persons, is often very sensitive or 
" ticklish," and the mere exposure of the skin to the air of the room, 
coupled with the fear of examination, may cause great rigidity of 
the belly wall without there being any abnormal condition present. 
This can be generally overcome by gentleness in palpation and 
by resting the palm of the hand on the belly and partly flexing 
the ringers, rather than by attempting to insert the ringer tips 
between the abdominal muscles. 

Great resistance of the rigid abdominal muscles is found whenever 
peritonitis is present in an acute form, in some cases of renal and 
hepatic colic, and more commonly in lead colic and in hysteria. 
In acute peritonitis great tenderness to the slightest touch is also 
present. Another symptom of acute peritonitis, aside from the 



3io 



THE ABDOMEN AND THE ABDOMINAL VISCERA 



exquisite tenderness of the abdomen, the drawn lip, the thirst, 
and the distention or rigidity of the belly wall, is pain of a severe 
character; unless it be septic peritonitis, when pain may be absent. 
There are also the drawing up of the limbs to relieve abdominal 
tension, obstinate constipation, moderate fever, and a very rapid, 
quick pulse. The tongue speedily becomes dry and parched, and 
collapse may soon ensue in severe cases. It is not to be forgotten 




Fig. 119. — McBurney's point of great tenderness in appendicitis. 



that localized peritonitis may result from many causes, usually 
from disease of the appendix vermiformis or the genito-urinary 
tract in women, and that the local symptoms and lesions may be 
limited by a wall of lymph to a very small area of the abdominal 
cavity. 

In appendicitis, rigidity may be general if the inflammation is 
widespread, or localized in the right iliac region if the original area 



SWELLING OR TUMOR IN THE UPPER ABDOMINAL SEGMENT 31I 

is limited or walled off from the rest of the abdominal cavity. If 
the rigidity be due to peritonitis, secondary to appendicitis, the 
following symptoms will point to an inflammation of the appendix 
as the cause: 

There is usually a rapid pulse, which becomes more and more 
speedy as the gravity of the case progresses. Indeed, a very rapid 
pulse is a sign of great importance as indicative of the severity of 
the malady. There is marked tenderness at McBurney's point 
(Fig. 119) on pressure with the finger tip. The pain may be referred 
to the epigastrium and the sigmoid flexure as well, but is not so 
severe on deep pressure in these parts. There is often an increased 
leukocytosis, an anxious face, and sometimes very great pain. 
(See chapter on Pain.) Febrile movement is usually moderate, 
and it may be absent. It is to be constantly borne in mind that 
the early stages of typhoid fever often so closely simulate appen- 
dicitis of the subacute type, that a differential diagnosis can only 
be reached after a most careful study of the case. 

Other conditions which simulate appendicitis are right-sided 
pleurisy, cholecystitis, gastric and duodenal ulcer, psoas abscess, 
and renal colic. All of these states cause at times abdominal 
rigidity, and one or more of the other signs of appendicitis. (See 
chapter on Pain.) 

Swelling or Tumor in the Upper Abdominal Segment. — Let us 
suppose that on placing the hand upon the epigastrium and the 
upper part of the umbilical area we find a swelling, an abdominal 
tumor. In the first place, we must decide as to whether it is in the 
abdominal wall or in the abdominal cavity. If it is in the wall, it 
will be movable with the tissues of the wall and readily grasped by 
deep palpation; but if in the abdominal cavity the abdominal wall 
may be made to move over it unless it be attached to the parietal 
peritoneum. 

Let us suppose it is in the wall of the abdomen, What can the 
swelling be? It may be a fatty tumor; in which case its surface 
will be dimpled and resistant, probably not painful, unless the 
part has been inflamed by rubbing or an injury, and it will not 
fluctuate. There will generally be a history that the person has 
exercised constant pressure on the part, as in leaning against a 
bench or table. Again, it may be an abscess; but aside from the 
rarity of this condition, we can exclude such a possibility by the 
absence of pain and fluctuation, and the absence of a history of a 
severe injury. 

Very much more commonly a swelling in the epigastrium, or 
upper umbilical area, is due to an intra-abdominal cause. In adults 
the most common cause is probably a growth (generally a car- 
cinoma) of the pyloric end of the stomach, to an indurated gastric 
ulcer, or to disease of the gall-bladder. In other instances it is due. 



312 THE ABDOMEN AND THE ABDOMINAL VISCERA 

particularly in children, to enlarged lymphatic glands, as in tuber- 
culous disease of the mesentery. Carcinoma of the pancreas may 
also cause a swelling in this neighborhood, or a cyst of the pancreas 
may be present. Aneurysm of the abdominal aorta is also not to 
be forgotten, but while any growth in the middle line may transmit 
the aortic impulse in aneurysm, only an aneurysm gives expansile 
pulsation. 

If the growth be gastric carcinoma, the patient will be in or past 
middle life (probably between the fortieth and seventieth years, 
although cases may occur as early as thirty years); will have 
a history of constantly increasing discomfort in the stomach; 
there will have been much belching, and perhaps vomiting of 
coffee-ground-looking material; marked loss of flesh and some 
cachexia may be present. The disease occurs twice as frequently 
in men as in women. According to Welch's statistics, out of 1300 
cases of gastric cancer, 791 were in the pylorus, 148 in the lesser 
curvature, 104 in the cardia, 68 in the posterior wall, and 61 
involved the whole stomach. The growth, if in the pylorus, 
is usually freely movable, and for this reason can be readily 
felt, and then is often momentarily lost to palpation. Its position 
is apt to change with the posture of the patient and the presence 
or absence of food in the stomach. Pain is usually elicited on deep 
pressure, and, if the growth be large and at the pylorus, the 
symptoms of dilatation of the stomach may be present, because 
that viscus is dilated through obstruction of the pyloric opening, 
which results in retention of the gastric contents. (See Gastric 
Dilatation, p. 304.) 

Similar symptoms may, however, be produced by a deposit of 
inflammatory lymph around a pyloric ulcer, which being changed 
into fibrous tissue, causes great thickening of the gastric wall with 
matting of the omentum around it, closely simulating the mass 
produced by a malignant growth or simple hypertrophic pyloric 
stenosis. When cancer involves the cardiac area of the stomach, 
this organ, instead of becoming dilated, becomes greatly diminished 
in size, and feels like a narrow band in the neighborhood of the 
left floating ribs and epigastrium. The diagnosis will be aided by 
discovering that the capacity of the stomach is very small and 
hydrochloric acid greatly decreased. 

But the presence of a tumor which can be palpated in the neigh- 
borhood usually occupied by the stomach does not, of necessity, 
indicate that this viscus is diseased. Not very infrequently an 
abnormal position of the colon or of other portions of the viscera 
may result in the physician's mistaking a growth in these parts 
for a gastric cancer. Even carcinomatous lymph nodes may lead 
to this error. 

In considering the differential diagnosis of carcinoma of the 



SWELLING OR TUMOR IN THE UPPER ABDOMINAL SEGMENT 313 

stomach and bowel, it is to be remembered that the former is far 
more common than the latter. Thus Heimann found that out of 
20,054 cases dying of carcinoma in the hospitals of Prussia, 10,537 
involved the digestive tract, and of these, 4288 affected the 
stomach, whereas only 20 involved the small intestine and 224 
the large intestine. 

Sometimes in cases of chronic gastric ulcer the area involved 
becomes so indurated as to be felt as a hard mass through the 
abdominal wall. In such instances the points which aid us in 
separating the condition from gastric cancer are the fact that the 
patient is young and usually a woman; and that the vomiting 
occurs immediately after taking food, for in gastric cancer it is 
seen in most cases several hours after food has been taken. As 
a rule there is no cachexia in cases of gastric ulcer, though there 
may be marked anemia. There is usually in cases of ulcer no great 
loss of weight unless the symptoms have been present a long time. 
In gastric ulcer vomiting of bright blood may occur, whereas in 
gastric cancer if blood is present it is broken-down blood and 
resembles coffee-grounds. Coffee-ground vomit often occurs in 
ulcer, however. 

In cases of gastric ulcer great pain is often produced by deep or 
even superficial pressure over the epigastrium, and a painful spot 
can generally be found on the back, about the angle of the right 
scapula. 

These painful spots are, however, as a rule, quite localized, and 
the fact that they are very painful at one particular spot, and 
yet the surrounding parts are comparatively insensitive, points to 
ulcer as a cause. 

It is worth remembering, however, that duodenal ulcer may 
cause identical symptoms subjectively and on palpation, and the 
history that the patient has passed dark, tarry stools, or that he 
has occult blood constantly in his stools confirms this diagnosis. 

The following table, slightly modified as to duodenal ulcer and 
its locality, has been devised by E. A. Codman. Certain of its 
statements taken by themselves, as he recognizes, are somewhat 
dogmatic : 



314 THE ABDOMEN AND THE ABDOMINAL VISCERA 



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SWELLING OR TUMOR IN THE UPPER ABDOMINAL SEGMENT 315 

Diffuse tenderness in this area may be due to colitis or even to 
appendicitis or sigmoiditis. 

The presence of a resisting mass, deeply situated in the epi- 
gastrium, or the upper part of the umbilical area, and felt only 
on deep palpation, and then often indistinctly, should bring before 
the mind the possibility of the presence of carcinoma of the pancreas, 
a diagnosis which will be largely confirmed if cachexia be assert- 
ing itself, if there be pain in this neighborhood, and if there are 
oily stools after fats are taken, as a result of the absence of pan- 
creatic juice. Still further confirmation of this diagnosis will be 
present if diabetes mellitus develops (pancreatic diabetes). Such 
a growth in the pancreas is usually a scirrhous cancer, and may 
be primary or secondary. Stiller asserts that the following symp- 
toms are fairly sure signs of pancreatic cancer, namely, marked 
dyspepsia, rapid emaciation and cachexia, subnormal temperature, 
persistent and progressive jaundice without hepatic enlargement, 
but often with swelling of the gall-bladder from obstruction to 
its duct. These signs are, of course, only of value if the evidence 
of malignant growth elsewhere can be excluded. 

Not rarely a mass, or masses, are felt in the abdomen which may 
be due to tuberculosis of the mesentery, which causes a drawing up 
or puckering of the membrane, so that there can be felt a firm 
mass extending across the upper abdominal zone. Sometimes it 
can be felt to the right or left of the middle line. In other cases, 
but rarely, we find retracted and thickened coils of intestine which 
feel like tumor masses, and these are apt to be drawn against the 
spine, so that the belly is very scaphoid and empty. We also 
meet with cases in which large tuberculous growths of the mesen- 
teric glands occur. In the last group of cases and in those of the 
omental type, named above, there may be some ascites. 

Either palpation or inspection may reveal pulsation in the 
epigastric area. This may be due to distention or enlargement 
of the right ventricle or to excessive aortic pulsation or to venous 
pulsation in the liver. If due to a transmitted impulse from the 
ventricle there will be additional signs of cardiac disturbance on ex- 
amining the heart, and in actual hepatic pulsation there will be found 
not only tricuspid regurgitation, but a pulsation below the floating 
ribs at the lower border of the liver. An excessive aortic pulsation 
is often met with in hysterical or neurasthenic persons without any 
abdominal lesion. Epigastric pulsation is also often transmitted 
from the aorta to the hand by enlarged abdominal glands or tumor 
masses. If the pulsation of the aorta is not transmitted by glands 
or tumors, the impulse may be due to aneurysm of the abdominal 
aorta, the diagnosis of which is established if, in addition to a 
pulsation, we also find on palpation a marked thrill, an expansile 
movement of the tumor, and, on auscultation, a bruit. Pain 



316 THE ABDOMEN AND THE ABDOMINAL VISCERA 

due to pressure of the aneurysmal sac upon some of the nerves of 
the abdominal cavity may also be a prominent symptom, but it 
should be remembered that aneurysm of the abdominal aorta is so 
rare that the law of probabilities is always against its presence. 
Sometimes a horseshoe kidney extending across the vertebral 
column will mislead one into a diagnosis of an intra-abdominal 
tumor, for horseshoe kidney is not very rare, being found as often 
as once in 1650 autopsies. 

Tumors or foreign bodies in the bowel can nearly always be moved 
about unless bound down by inflammatory adhesions, so differing 
from growths which involve the immovable parts, such as the retro- 
peritoneal glands. Very rarely we find a cancerous tumor of the 
omentum, but when it is present it usually becomes retracted and 
indurated, so that its hardened edges can be felt extending across 
the abdominal cavity. More commonly when multiple nodules 
are found in the omentum or studded over the surface of the bowels, 
they are due to peritoneal tuberculosis. Not rarely these nodular 
masses are also found studded over the mesentery. 

Localized masses due to other causes than those already dis- 
cussed are due to impaction of feces, volvulus, and intestinal 
obstruction, from other causes, as, for example, cancer of the bowel. 
(See chapter on Vomiting.) Such a growth occurs most frequently 
in the cecum, when the tumor will be found in the right groin, or in 
the sigmoid flexure, when it will be found in the left groin. 

The appearance of sudden swelling in the neighborhood of the 
pancreas, associated with intense pain, nausea, and vomiting, may 
be due either to acute hemorrhagic pancreatitis, to hemorrhagic 
infarction of the intestine, to intestinal obstruction, acute chole- 
cystitis, or to acute peritonitis resulting from perforation of the 
stomach or duodenum. (See Pain.) The last three are the more 
common. An exploratory operation is the only way of deciding 
the diagnosis positively, although the history of the patient may 
aid us in deciding the cause of the illness. Thus, if there is a history 
of gall-stone colic, this may indicate that a stone has become 
impacted in the common duct near the papilla, and such an accident, 
if it dams back the secretion into the pancreas, causes hemorrhagic 
pancreatitis with fat necrosis. Sometimes, however, the symptoms 
of hemorrhagic pancreatitis are more prolonged, and life lasts for 
several weeks, local swelling, jaundice, and pain being present, 
with symptoms of suppuration. 

Very rarely swelling in the epigastric region, either rapid or slow 
in onset, follows upon the formation of cysts in the pancreas, as a 
result of obstruction of a duct of the gland. When they occur, 
these cysts may be very large, although, as a rule, they are small. 

As pointed out, however, by Jordan, the cause of a swelling in 
the pancreatic region may be hemorrhage into the lesser peritoneal 



SWELLING OR TUMOR IN THE UPPER ABDOMINAL SEGMENT 317 

cavity. He summarizes some of the points in regard to this matter 
as follows: 

" Contusions of the upper part of the abdomen may be followed 
by the development of a tumor in the epigastric, umbilical, and left 
hypochondriac regions. Such tumors may be due to fluid accumu- 
lating in the lesser peritoneal cavity, and when the contents are 
found (on aspiration) to have the power of converting starch into 
sugar we may assume that the pancreas has been injured." Finally, 
Jordan states that "many such tumors have been regarded as true 
retention cysts of the pancreas." 




Fig. 120. — Showing percussion dulness of liver and heart. 

Disease in the right hypochondrium, when not due to a lesion 
of the pylorus, may arise from changes in the liver. Normally, 
in the adult, this gland cannot be felt below the ribs, except part 
of the left lobe in the epigastrium occasionally, although sometimes, 
on deep inspiration, the diaphragm pushes the liver low enough 
to be felt. In children the liver is naturally large enough to be 
felt below the ribs. 

When the normal liver is percussed we find that it lies in the area 
shown in Fig. 120, and that as we percuss above it on the ribs in 
the mammary line we first get pulmonary resonance; then a little 
below this, impaired resonance, due to the fact that the lower edge 



318 THE ABDOMEN AND THE ABDOMINAL VISCERA 

of the lung is interposed between the chest wall and the liver; and 
still lower we find absolute dulness or flatness, due to the solid 
liver itself. Below this area, which ceases just below the lowest 
rib, we usually find tympany on percussion, due to the gas-dis- 
tended bowel. If we percuss in the midsternal line, we get the same 
signs; but they begin as high as the nipple, or above it, and then 
cease at a line drawn across the abdomen about the level of the 
ensiform cartilage. To the left of the middle line of the sternum 
the liver dulness merges into the cardiac dulness (Fig. 120). In the 
mammary line liver dulness begins at the fifth rib, laterally it 
begins at the seventh and eighth, posteriorly at the tenth rib, 
owing to the sloping of the diaphragm. 

When a hard and firm mass with a smooth surface can be felt 
in the right hypochondrium or right umbilical area, which is 
movable, and which has an edge which can be readily felt on deep 
palpation, particularly when the patient takes a long-drawn, deep 
breath, the mass is probably an enlarged liver or a liver pushed 
down into the abdominal cavity by a large pleural effusion, an 
emphysematous lung, pneumothorax, or rarely, a subphrenic 
abscess. The causes of enlargement are congestion, due to cardiac 
disease, hypertrophic cirrhosis, abscess, carcinoma, sarcoma, 
lymphadenoma and amyloid degeneration. When the surface is 
found to be smooth, the condition is probably congestion, hyper- 
trophic cirrhosis, amyloid or fatty degeneration. If the surface 
is rough, it will probably be due to atrophic cirrhosis, which 
gives a granular sensation to the hand when the abdominal wall 
is moved over the organ, but the liver is often so small in this state 
that it cannot be palpated except in emaciated persons. In malig- 
nant growth large and small nodules may often be found, and 
depressions or umbilications of its surface may be noted, but it 
must be remembered that cancer of the liver is not necessarily 
associated with the presence of nodular masses. On the contrary, 
the growth or growths may be large, yet project so slightly above 
the hepatic surface that they cannot be felt. In such cases there 
may be pain, marked emaciation, cachexia, and the organ is found 
much enlarged. 

The physician who feels distinct nodules on the surface of the 
liver should not immediately conclude that these are necessarily 
carcinomatous, for syphilis often produces a very extraordinary 
nodulation of the surface of this organ. So great is this, that when 
nodulation is excessive the possibility of syphilis being the cause 
is to be considered. This form of disease is, however, rarely 
accompanied by as great hepatic enlargement as is that due to 
cancer with marked and multiple nodules. 

The consistency of the liver is usually very hard in cases of cir- 
rhosis, carcinoma, and amyloid degeneration. In atrophic cirrhosis 



SWELLING OR TUMOR IN THE UPPER ABDOMINAL SEGMENT 319 

there will be some ascites in many cases, some swelling of the legs per- 
haps, and dull pain in the hepatic region. The digestion will be dis- 
ordered, there will be marked loss of flesh, and often hematemesis. 
In cases of cirrhosis of the liver, whether it be in the hypertrophic 
or atropic form, the patient rarely complains of the organ, and no 
symptoms which seem to him hepatic in origin may be present, save 
that in the hypertrophic state its size is increased, so that it can be 
felt below the ribs, whereas in the atrophic state it cannot be felt 
except by pushing the fingers well up under the ribs. The symptoms 
accompanying cirrhosis are chiefly connected with disorders of the 
alimentary canal, either through direct failure in the digestion and 
assimilation of food, or from changes in the blood supply of the 
abdominal contents. The following excellent diagram, from Sey- 
mour Taylor's Index of Medicine, shows what these symptoms are, 



Liver 



Morning Sickness 

Hozmatemesis 

Dyspepsia 




(Pallor, Pain 
Spleens and 

[Enlargement 



Fig. 



Hemorrhoids 
121. — To illustrate symptoms of cirrhosis of liver. (Seymour Taylor.) 



and discovers their cause at a glance, the cirrhotic process, of course, 
obstructing the flow of blood in the liver (Fig. 121). It is a note- 
worthy fact that in the atrophic form jaundice is rare even in the 
very last stages of the disease, whereas in the hypertrophic form 
it is commonly met with, because in the former the fibroid changes 
chiefly involve the bloodvessels, whereas in the latter the biliary 
radicles are affected. Ascites is common in the atrophic form, 
rare in the hypertrophic variety for these reasons. In the case 
of amyloid liver there will be a history of prolonged suppuration 
elsewhere, and there will be present disordered digestion, irregular 
bowel movements, and little pain. 

Tenderness of the right hypochondrium is usually found in 
congestion of the liver, commonly due to heart disease, in inflam- 



320 THE ABDOMEN AND THE ABDOMINAL VISCERA 

mation of its tissues, such as that caused by an infection resulting 
in cholangitis, and in malignant growth. Tenderness is practically 
absent in amyloid liver and in fatty degeneration. 

Sometimes enlargement of the liver and ascites are due to 
adhesive pericarditis. The diagnostic signs of adhesive pericarditis 
consist in systolic retraction of the intercostal spaces in the anterior 
axillary line, and posteriorly at about the fifth or sixth rib on the 
left side, which retraction is followed by a diastolic rebound. If 
the patient is told to forcibly inspire or expire, the natural change 
in the position of the apex beat of the heart in relation to the chest 
wall does not occur, neither does the edge of the lung on full in- 
spiration diminish the area of cardiac dulness as it does in health. 
Pericarditis with ascites is often associated with hyperplastic peri- 
hepatitis, the "iced liver" of Curschmann. 

The physician who finds the lower margin of the liver abnormally 
low down in the abdominal cavity should not make a diagnosis of 
enlargement of this organ until he has assured himself that the 
extension of the margin of the liver is not due to an effusion in the 
right pleural cavity which presses upon this organ. So, too, if the 
patient is a woman, the lower border of the liver may have been 
pushed down by tight lacing, and careful palpation may reveal a 
furrow across its surface produced by the corset. Finding the lower 
border of the line abnormally low down is, however, indicative of 
enlargement if careful percussion shows that the upper border of 
liver dulness is in its normal place. If the upper border of the 
liver is below the normal level and pleural effusion and subphrenic 
abscess are excluded, it is a sign of floating liver. 

When, on palpating the liver, we find marked tenderness and 
some swelling, and, associated with these symptoms, fever, rigors, 
sweats, and sometimes vomiting, and, in addition, a history that 
the patient has had dysentery or has been in the tropics, or has 
swallowed bad water, the presence of an abscess of the liver is 
indicated. This may be single or multiple. If the latter, it is 
probably due to pyemia, and no spot of fluctuation will be found, 
as a rule; whereas, if it is large and single, fluctuation is sometimes 
felt. Further, the enlargement of the liver in the pyemic form is 
uniform, whereas in the single abscess there is often one spot which 
is swollen or enlarged. The history of the case will usually sepa- 
rate the conditions, one from the other, for diagnostic purposes, 
for in the cases of abscess the history will probably be that 
of a person exposed to an amebic dysentery or one who has 
had an acute infection. The possibility of a suppurating gall- 
bladder, and of cholangitis, is not to be forgotten in such a case. 
More rarely a single hepatic swelling may be due to hydatid cyst, 
but the absence of septic symptoms the history of the case, and 
presence of fluctuation, combined with the result of examining 



SWELLING OR TUMOR IN THE UPPER ABDOMINAL SEGMENT 32 1 

the fluid aspirated from the swelling, will decide the diagnosis. 
Fuither than this, hydatid cyst yields on percussion a peculiar 
vibratory thrill called the hydatid thrill. Three fingers are placed 
over the area, the middle one being pressed firmly upon the growth 
and the lateral ones but lightly. The middle finger is now per- 
cussed and allowed to remain in situ, when an after-thrill may be 
felt in the other fingers. 

A much more frequent lesion in the right hypochondrium or 
epigastric area, or so near to it as to lead the physician to consider 
it epigastric, is disease of the gall-bladder. Theoretically the area 
of the gall-bladder is distinctly to the right of the median line, but 
in women whose lower ribs have been compressed by corsets the 
gall-bladder is pushed inward, and, it may be, distinctly downward. 
Because of these facts, and because carcinomatous disease of the 
stomach and gall-bladder have a direct etiological relationship, the 
possibility of an epigastric mass being a gall-bladder growth must 
always be considered. As a rule, however, disease of the gall- 
bladder is discovered while palpating the lower border of the liver. 
If the mass is of good size and the abdominal wall thin, it will be 
felt as a pyriform body and may be slightly fluctuating. Such a 
mass is probably a distended gall-bladder, and it may be associated 
with enlargement of the liver and jaundice. 

The causes of enlargement of the gall-bladder are several, viz., dis- 
tention from the accumulation of bile produced by obstruction in 
the cystic or common duct, or the presence of a large number of 
calculi in the gall-bladder, and often to the accumulation of thin 
mucus, which may or may not be bile-stained, the so-called 
" hydrops of the gall-bladder." The causes of acute obstruction 
of the ducts are gall-stones, new growths, such as carcinoma and 
rarely gumma, and inflammatory processes in the ducts them- 
selves, with inflammation in surrounding tissues and organs. 
Often the inflammatory processes just named will have been pro- 
duced by the presence of gall-stones, which may, by causing ulcera- 
tion of the mucous membrane, permit severe infections to take 
place. 

Obstruction of the bile ducts may be, as already stated due to 
stone. If this is the cause, the patient may give the history that 
at some time in the near or remote past, after a period of more or 
less distress in the hypochondrium, she has been seized by a pain 
which was paroxysmal in type and extended backward and upward 
to the region of the scapula or shoulder. This pain was also pecu- 
liar in that it was apt to occur at night rather than after taking food, 
as in gastric cancer or ulcer. There may be, but often there is not, a 
history of jaundice. Manifestly this is a history of an attack or 
attacks of gall-stone colic, and should lead us to the belief that the 
enlargement of the gall-bladder is due to stone, but it may be due 



322 



THE ABDOMEN AND THE ABDOMINAL VISCERA 



to a malignant growth. In this connection it is well to take into 
consideration the importance of the presence or absence of jaundice, 
which is well expressed by Mayo Robson in the words: "Jaundice 
with distended gall-bladder is presumptive evidence of malignant 
disease, but jaundice without distended gall-bladder favors the 
diagnosis of cholelithiasis." This is sometimes called " Courvoisier's 
law." In other instances there may be no history of attacks of 
gall-stone colic, the patient simply complaining of pain and dis- 
comfort in the hepatic area. Not rarely these attacks of pain are 
regarded by patient and physician as being due to indigestion, 
gastric or intestinal. (See chapter on Pain.) 

It is important to remember that in some cases of enlargement of 
the gall-bladder due to obstruction of its duct the enlargement 
may be so gradual and so great that the distended viscus may be 
felt far from its normal site in the middle line or even under the 
left ribs. 



Compressed 
lung 



Apex beat 
not greatly 
displaced. 




Fig. 122. — Left pyopneumothorax subphrenicus. (After Maydl.) 



An additional symptom favoring gall-stone as a cause is fever, 
which is due to infection produced by the stone injuring the 
mucous membrane. Sometimes it is simply an indication of 
inflammation, at others it indicates anything from mild purulent 
infection of the bile passages to empyema of the gall-bladder or a 
general cholangitis. If the infection be with a benign organism, the 
symptoms may be mild; but if it be due to the more malignant 
forms it is often virulent, and the febrile movement most severe. 



SWELLING OR TUMOR IN THE UPPER ABDOMINAL SEGMENT 323 

Much depends, too, upon the freedom of drainage. If the gall 
duct permits the escape of the pus into the gut, the symptoms 
may become greatly reduced; but if it be retained they are apt 
to become more pressing and demand immediate surgical inter- 
ference. (See Cholecystitis, in chapter on Fever.) 

When the gall-bladder is distended with gall-stones there is often 
a history of colic ; there may be gall-stone crepitus on careful palpa- 
tion. It is not to be forgotten that gall-stones are present in about 
10 per cent, of all adults, although, as Kehr has well pointed out, 
fully 95 per cent, of such persons come to autopsy from other causes 
without even suffering from any manifestation of their presence. 
It is only when the calculus produces irritation or mechanically 
blocks the ducts that symptoms develop. 

In other instances a swelling in this neighborhood may be due 
to what is called pyopneumothorax subphrenicus, a condition of 
abscess in the peritoneal cavity below the diaphragm, produced by 
perforation of the stomach or transverse colon, the gall-bladder, or 
appendicitis. A history of gastric ulcer or gastric carcinoma or 
gall-bladder disease will aid in indicating the character of the lesion. 
The abscess so produced may contain gas, and for this reason the 
swelling may be quite resonant on percussion (Fig. 122). Abscess 
in this region also follows abscess of the pancreas or fat necrosis of 
this organ in rare instances. 

Floating kidney may also cause a marked movable swelling or 
tumor-like mass in the upper zone of the abdomen. It may be 
mistaken for a tumor of the liver, omentum, ovary, or spleen, or 
even for a much distended gall-bladder. If the belly walls are 
thin, the peculiar shape of the kidney can be outlined by palpation, 
and even the pulsation of the renal artery can be felt; but, as a rule, 
this cannot be done, and the dilatation of the pelvis of the kidney 
by the obstruction of the ureter, which has become twisted, may 
distort the shape of the organ. Deep palpation of the flank, if the 
kidney has floated away from its normal seat, may reveal lessened 
resistance in this area, and bimanual palpation, one hand being 
placed at the back and the other in front, may reveal the presence 
of the organ elsewhere. Further, if the patient be made to lie on 
the opposite side, the dislocated kidney may sometimes be clearly 
outlined by bimanual palpation. In other instances, the patient 
lying on the back with the thighs flexed, the physician lightly 
grasps the side close to the last rib and directs the patient to 
take a full breath, when the kidney, if movable from its normal 
resting place, may be felt passing down between the thumb in 
front and the fingers behind. The fingers should be in the flank 
and the thumb over the side of the abdomen (Fig. 123). If the 
kidney which has slipped down be pressed upon gently with the 
fingers of the free hand, it can be felt slipping into place. In other 



324 THE ABDOMEN AND THE ABDOMINAL VISCERA 

instances the patient stands erect, and the physician places the 
ringer tips of the left hand in the lumbar region, and pressure is 
made toward the front of the body. The ringers of the right hand 
are placed anteriorly, and pressure is made backward and upward 
so as to engage the kidney between the finger tips of the two hands. 
The vertical posture of the body aids in displacing the kidney, 
which may stay in place in the dorsal decubitus. The kidney may 
slip with a jerk, if already displaced, back into its normal position; 
or, if in place, it may be felt to escape downward into the abdominal 
cavity. Pressure on a floating kidney causes a peculiar nauseating 
pain somewhat resembling that produced by squeezing a testicle, 
and when the organ is caught between the hands it slips from the 
pressure with a sensation resembling that felt by the fingers when 
an orange seed is pressed between the fingers and thumb and 




Fig. 123. — Method of examining for floating kidney. The physician grasps 
the side with his hand in such a way that the fingers and thumb are approximated, 
and when the patient takes a full breath the kidney can be felt slipping through 
between the fingers and thumb. 

escapes the pressure. The condition of floating kidney is more 
common in women than in men, but it occurs in both sexes. In 
667 cases, 583 occurred in females and 84 in males (Kuttner). 
It is generally the right kidney which is displaced, although dis- 
location of the left kidney is not very rare. In Kuttner 's 727 
cases it occurred on the right side in 553, on the left in 81, and 
both sides in 93. Sometimes violent attacks of renal pain occur in 
cases of floating kidney. These have been called Dietl's crises. 
(See chapter on Pain.) 

When the kidney is enlarged from cystic degeneration, from 
ordinary hydronephrosis, and from echinococcus cysts, it may 
be readily felt even in the umbilical area. 

Hydronephrosis has been mistaken, in children particularly, for 
sarcoma of the kidney, and in adult females for ovarian tumor. The 
diagnosis in some of these cases can be made by the use of the x-rays 



SWELLING OR TUMOR IN THE UPPER ABDOMINAL SEGMENT 325 

or by tapping. The fluid obtained in hydronephrosis will usually be 
somewhat turbid and contain epithelial cells. It should not be for- 
gotten that the condition of hydronephrosis may be intermittent, for, 
if this is not remembered, the physician may be misled into thinking 
that the disappearance of the swelling is due to a floating kidney slip- 
ping back into its place. This variation in the size of the tumor may 
be of considerable diagnostic aid, for sudden decrease in size would 
indicate the escape of fluid through a temporarily patulous ureter, 
and its redevelopment would indicate that this pathway of escape 
was again closed. Should the fluid escape into the bladder free 
urination would naturally take place shortly after the tumor 
decreased in size. Hydronephrosis may be bilateral. In 13 out 
of 20 cases collected by Roberts this was the case. Severe pain is 
often a symptom of intermittent hydronephrosis. Pyelonephritis 
and pyelonephrosis may closely simulate hydronephrosis, but fever 
and the presence of pus in the urine will aid in making the differ- 
ential diagnosis. 

Bulging of the flank, with pain, fever, and perhaps fluctuation, 
indicates perinephritic abscess or caries of the spine with cold abscess. 

A fluctuating swelling in the epigastrium or flank may also 
arise from cysts of the mesentery. These may grow to a very large 
size. In other cases a cystic hydroma of the tissues near the kidney 
may be present. Hawkins has recorded a case in which a large 
cyst, with an atrophic third kidney attached to it, filled nearly the 
entire right side of the belly, and from which after death five pints 
of clear fluid, devoid of albumin and casts, were removed. As 
already indicated, much diagnostic aid can often be given by 
tapping an obscure abdominal cyst with a very fine needle. 

J. G. Clark has recommended a method of separating solid from 
fluid tumors, which is called trimanual percussion. This consists 
in fixing the mass between two hands, one below it if possible, the 
other above it. An assistant now percusses, striking the finger of 
the physician. By this means a thrill can be felt which would 
otherwise be lost. 

" Phantom tumor" is generally found in hysterical women, and 
often leads to ludicrous errors in diagnosis. It is due to presistent 
dilatation of a knuckle of intestine by gas, thereby forming a 
moderately hard and more or less constant mass, which may 
resemble a real tumor. Examination of the patient under ether 
will usually reveal its true character. This state is to be differ- 
entiated from what Nothnagel has called " intestinal rigidity." In 
this condition a knob projects through a thin anterior abdominal 
wall and gradually grows larger until, in the course of a few 
moments, it sinks out of sight and touch. It is a disorder of peris- 
talsis. Localized superficial and inconstant tumors may arise 
through spasmodic, but localized, contractions of the recti muscles. 



326 



THE ABDOMEN AND THE ABDOMINAL VISCERA 



Finally, a swelling in the neighborhood of the umbilicus should 
always arouse the suspicion of an umbilical hernia. The situation 
of the swelling at the umbilicus, the fact that percussion over it 
gives a highly tympanitic note, owing to the gas in the prolapsed 
gut, and the possibility of reducing its size by taxis in some cases, 
will render a diagnosis of umbilical hernia possible. 

In the left hypochondrium the spleen can be very readily outlined 
by percussion in persons not inordinately fat. Its normal position 
is best shown in Fig. 124. 

The upper border of the spleen is on a level with the ninth rib. In 
percussing the spleen heavy percussion is to be avoided, since this 

may develop the resonance of the stomach 
or bowels. The spleen cannot be palpated 
unless greatly enlarged, but it may be 
found bulging from beneath the lowest rib 
in typhoid fever; in scarlet fever; as the 
result of acute or chronic malarial fever 
("ague cake"); in leukocythemia of the 
splenomedullary variety (see Fig. 118), 
in amyloid disease, as that after long 
suppuration; in early syphilitic infection; 
and in any disease which causes venous 
engorgement of the abdominal viscera, 
such as cardiac failure or hepatic cirrhosis. 
The symptoms of splenomedullary leuke- 
mia are pallor and puffiness of the face, 
dyspnea, and general feebleness, with 
great and gradual enlargement of the 
spleen and liver, and marked splenic ten- 
derness. Auscultation over this organ 
may reveal a murmur and palpation a 
crepitus. Hemorrhage, generally from the 
nose, is common, and dyspnea and diarrhea 
are often present. Frequently retinitis de- 
velops, and slight fever may occur. This is 
by far the more common form of leukemia. 
The spleen sometimes reaches a very large size in the disease 
which has been called " splenic anemia," one form of which is 
called Banti's disease. The blood, unlike that in true leukemia, 
does not show great changes in the white cells save a leukopenia. 
The red cells are greatly decreased in number. This disease is 
divided by Banti into three stages: the stage of anemia char- 
acterized by enlargement of the spleen, and lasting from three 
to ten years; a transitional stage; and a third stage of marked 
ascites, which usually terminates in a few months. In some 
cases of so-called Banti's disease, hemorrhages take place, such as 
vomiting of blood; nose-bleed, hemoptysis, and hematuria. 




Fig. 



124. — Normal position 
of the spleen. 



SWELLING OR TUMOR IN THE UPPER ABDOMINAL SEGMENT 327 

Sometimes displacement of the spleen downward arises from 
emphysema of the lungs or left-sided pleural effusion. 

Nearly always the splenic surface is smooth, except for the 
notch in its surface, unless the disease be the rare condition of 
hydatid disease or carcinoma. 

In connection with the subject of abdominal tumors, we should 
not forget the possibility of a floating spleen, a rare condition, but 
one more common than is generally thought. The shape of .the 



§ ' X 



Fig. 125. — A case of chronic enlargement of the spleen following typhoid 
fever. The dark line shows the margin of the organ on palpation, while the 
retraction in the line and the dotted line indicate the position of the splenic 
notch. (From the author's wards in the Jefferson Medical College Hospital.) 

organ, if it can be palpated, will aid the diagnosis, and the pres- 
ence of resonance on percussion over the area of normal splenic 
dulness will confirm the diagnosis that the spleen has become 
displaced. As the spleen in this condition may fall as low as the 
virgin uterus, it may simulate any growth from a uterine myoma 
to a tumor of the bowel or pancreas. By reason of twisting of its 
pedicle and secondary engorgement, its size may be enormous ; but 
if this condition continues, atrophy finally takes place. As such 



328 THE ABDOMEN AND THE ABDOMINAL VISCERA 

a dislocated spleen drags on the stomach and pancreas, it may 
cause a long train of curious symptoms, and even intestinal obstruc- 
tion. Sutton asserts that by pressure it may cause displacements 
of the uterus. 

Finally before dismissing the important subject of swelling and 
tumor in the upper abdominal zone it is necessary to recall the fact 
that because of the close juxtaposition of many organs in this area 
an exact diagnosis may be impossible, so far as a diagnosis of the 
actual lesion is concerned, and yet a sufficiently accurate diagnosis 
may be made to direct treatment. Thus a chronic inflammatory 
process about the gall-bladder may, by involving the pylorus in 
its adhesions and exudations, cause signs of gastric dilatation and 
obstruction, or again, a history which seems characteristic of gall- 
stone colic may be really due to ulcer of the pylorus. Further than 
this it is to be recalled that all these parts are in health quite 
movable and in disease are often found far from their normal sites. 
Thus the pylorus may be anchored high up in the belly by 
adhesions or dragged into the umbilical area by the weight of a 
growth. 

The Groins. — There yet remains for discussion the significance 
of increased resistance on palpation, and percussion dulness, in the 
groins. 

In the right iliac region the presence of swelling, increased 
resistance, impaired resonance, particularly if pain and tender- 
ness are present, point strongly to appendicitis or to inflam- 
mation about the caput coli. Sometimes, however, the presence 
of a distinct lump in this region in a person advanced in life may 
mean a malignant growth, for carcinoma of the caput coli is not 
rare. 

If the left groin is affected in a person well advanced in years, 
carcinoma is also to be regarded as possible, for the sigmoid flexure 
is a frequent seat of such a growth. In a young person or a child 
impaction of feces, a foreign body, and intestinal obstruction is also 
to be considered. (See chapters on Vomiting and on the Bowels.) 

For further information in regard to the diagnosis of diseases of 
the abdominal viscera, the reader is referred to the chapter on the 
Skin (that part on Jaundice), the chapter on Vomiting (that part 
on Intestinal Obstruction), to that on the Bladder and Urine, and 
to that on the Bowels and Feces. 



CHAPTER XI. 
THE BOWELS AND FECES. 1 

Constipation and diarrhea — -The cause of these two symptoms and their diag- 
nosis — The diseases in which these symptoms occur — Choleraic diarrhea — 
Dysentery — The color of the feces — Intestinal parasites. 

The consideration of the conditions of the bowels and feces as 
indicative of disease affecting the intestines themselves and other 
organs closely associated with them, can be best divided into 
several parts, namely, the functional disorders of the intestines 
and the organic diseases from which they may suffer, on the one 
hand, and the appearance of the feces in both functional and 
organic diseases of the abdominal viscera in general, on the other. 
The most common forms of intestinal disturbance are constipation 
and diarrhea. 

Constipation. — Constipation may be due to mere sluggishness of 
bowel movement because of both nervous and muscular atony, or to 
deficient secretion of the intestinal juices, or, again, to the too rapid 
absorption of the liquids from the fecal matter while it is passing 
through the colon. It is also associated with all those conditions 
which prevent the proper flow of bile, which liquid very materially 
increases peristalsis. Thus, we see obstinate constipation in most 
cases of true jaundice; in cases of hepatic disease, producing a defi- 
cient biliary flow; and in phosphorus poisoning, in which the fatty 
degeneration and hepatitis prevent biliary secretion. Further than 
this, the constant ingestion of foods which are absorbed nearly in 
toto, or, in other words, leave little residue, particularly raw or 
boiled milk, produces constipation. Again, the use of wines con- 
taining large amounts of tannic acid may produce similar results 
because of the astringency of this substance, and chronic constipa- 
tion from the use of large quantities of badly infused or boiled 
tea made with hard water is frequently met with. 

When the feces are very dry, the cause may be lack of liquid 
ingested, and the remedy be full draughts of pure water; or, 
again, constipation occurs as a manifestation of diabetes insipidus 
or diabetes mellitus, because the polyuria characteristic of these 
affections drains the body of liquid. Obstinate constipation 
should, therefore, always call the physician's attention to these 
affections and to two other possibilities, namely, that the con- 

1 For intestinal obstruction in its various forms, see chapter on Vomiting. 



330 THE BOWELS AND FECES 

dition depends upon wilful disregard by the patient of the calls of 
nature, so that the bowel is forced to retain fecal matter until it 
becomes hard and dry; or, quite as important, that the constipation 
may be due to some reflex cause, which, as the result of irritation, 
results in an arrest of peristaltic movement. Thus, a woman with 
ovarian and other pelvic trouble may have obstinate constipation 
which yields little, if at all, to purgatives, but readily to nervous 
sedatives or even to an opiate. Or, again, in chronic lead poison- 
ing the inhibitory fibers of the splanchnic nerves and the intestinal 
muscularis may be so irritated that peristalsis is impossible. Here a 
hypodermic injection of morphine may make a movement possible. 

The organic diseases of the bowel producing constipation are 
many and of great importance. They consist in intestinal obstruc- 
tion in all its forms, as by bands, growths, by the process of intus- 
susception, by volvulus, by cicatricial contractions, and by impacted 
foreign bodies or fecal matter. The presence of a sudden attack 
of constipation, in a degree which fails to yield to mild purgatives, 
should always put the physician on his guard lest some grave 
condition is present. As severe and, finally, stercoraceous, vomit- 
ing is a fairly constant and more characteristic symptom of intes- 
tinal obstruction than is constipation, a discussion of the various 
symptoms of intestinal obstruction will be found in the chapter 
on Vomiting, and the diagnosis of growths of the intestine will be 
found in the chapter on the Abdomen. 

Aside from these causes, it is manifestly impossible to discuss all 
the conditions of the system in which constipation may be present. 
The physician must always bear in mind that constipation often 
results in the absorption of poisonous materials from the bowels, 
which in turn may produce all sorts of symptoms, nervous or other- 
wise, such as severe headache and vertigo, with vomiting. 

Diarrhea. — Diarrhea of an acute type depends, as a rule, upon 
one of four causes, namely, the presence of irritant material in the 
bowel, which the intestines attempt to get rid of by increased 
secretion and excessive peristalsis; relaxation of the bloodvessels 
of the intestine, with profuse serous leakage and consequent watery 
purging; acute inflammation, with excessive secretion of mucus; and 
the endeavor of the system to eliminate poisons in this manner, 
as in cases of sudden profuse diarrhea, in cases of chronic renal 
disease, in which the purging is an effort of elimination. 

It is impossible to speak of all the possible causes of diarrhea, or 
of all the diseases in which it is met with. Only those in which it is 
a prominent symptom, or one of importance, can be discussed. 

One of these is cholera morbus, a disease which manifests itself 
in profuse watery purging, accompanied by violent pain in the 
belly, and, after several stools have passed, in a considerable 
amount of tenesmus. Mucus is almost entirely absent from the 



DIARRHEA 33 1 

dejecta, but particles of undigested food may be found in them. 
Vomiting is often a severe and simultaneous manifestation of the 
gastro-intestinal disorder which exists, and, if the attack be very 
severe, it is practically impossible to separate it from true cholera 
Asiatica if an epidemic of that disease is present. The patient 
speedily becomes cold and pinched-looking, exceedingly weak, 
and finally may pass into collapse. The pulse becomes feeble, 
rapid, and running; the face livid, and finally the patient may 
develop the fades Hippocratica. The urine is greatly decreased 
or entirely suppressed, because of the watery purging, and possibly 
by reason of the effects of certain poisons upon the kidneys. In 
the great majority of cases the symptoms are not so severe as this, 
and complete recovery ensues as soon as the offending materials 
are passed out of the bowels and the patient has time to convalesce. 

When an attack of diarrhea, such as has just been described, 
comes on in a young child it is usually called cholera infantum, or 
"summer complaint," and it is nearly always due to improper 
feeding or to the unintentional use of bad food or bad milk. The 
stools of the child are usually at first filled with curds of milk and 
green masses, looking as if the curds had been stained with grass 
juice or spinach. The child often passes with extraordinary 
rapidity into a state of collapse, and may die in a few hours or days. 
The tenesmus often becomes constant and is a distressing symptom, 
and the tissues become shrunken to a marked degree. The child 
manifests not only the evidences of the results of profuse purgation, 
but, in addition, is evidently intoxicated by the toxins absorbed 
from the bowel, so that it lies on the lap of the nurse in a relaxed 
and torpid state. The surface of its body is often abnormally cold, 
and its extremities may be pinched and blue; but the temperature 
of the internal organs is sometimes abnormally high, so that while 
the axillary temperature may be below normal, the thermometer 
will reveal a temperature of from 102 ° to 103 ° in the rectum. 
Sometimes the head becomes retracted, as if meningitis was 
present. The respirations may be sighing or of the Cheyne- 
Stokes type. 

If the child or adult is seized with symptoms such as those 
described under cholera morbus or cholera infantum, and a sus- 
picion of the presence of true cholera is raised, Are there any facts 
which will point to the correct decision in a case, even if, as already 
stated, a positive differential diagnosis cannot be made? In the 
first place, a train of symptoms of a malignant type points to the 
true cholera, rather than cholera morbus, or cholera nostras, as 
it is sometimes called. Again, the evidences of infection or general 
systemic disease indicate the epidemic malady rather than does a 
profuse diarrhea alone. Thus, the systemic signs of infection may 
be so great that death from infection in true cholera occurs before 



332 THE BOWELS AND FECES 

diarrhea even begins. Again, it would be possible to determine the 
presence of true cholera if the comma bacillus could be demon- 
strated; but this requires the examination of the fecal matter to 
be made by an expert who is familiar with the technique of examin- 
ing fecal matter for the germs and with the necessary measures 
for their artificial culture. 

Symptoms identical with the more violent forms of cholera 
nostras or true cholera may be produced by acute poisoning by 
antimony, except that in this case we often have profuse sweating 
and salivation early in the attack. The same symptoms of vomit- 
ing, purging of rice-water stools, collapse, cramps in the calves of 
the legs, and violent pain in the abdomen may be present. A 
differential diagnosis without the history of the patient having 
taken poison is impossible, except by a chemical analysis of the 
vomited matter, which will contain antimony, as will the stools 
and the urine. The utmost care should be used that the vessels 
which receive these materials are chemically clean, that they are 
hermetically sealed until ready for the expert analysis, and that 
they are in the hands of thoroughly responsible parties up to the 
date of analysis. 

While arsenic may cause somewhat similar symptoms to those 
due to antimony, the stools are generally bloody. Rarely certain 
poisonous toadstools produce somewhat similar symptoms. 

If an adult who has not eaten anything which could have pro- 
duced a diarrhea, as, for example, bad food, is seized with profuse 
watery purging, with very little or no pain, and without nausea 
and vomiting, it is probable that he is suffering from the acute 
nervous diarrhea which sometimes results from exposure to severe 
nervous strain. To illustrate the character of these cases the 
author may mention the fact that in the days of oral examination 
it was quite common for him to see medical students, exhausted 
by a long winter's work and anxious about their examinations, 
seized by an attack of profuse watery purging in the middle of 
the night preceding the examination of which they stood most 
in dread. 

In other cases profuse purging develops suddenly in hot weather 
as a form of heat prostration. 

Care must be taken by the physician in all cases of sudden and 
profuse diarrhea to which he is called to exclude the presence of 
renal disease, for purging may be an effort at elimination of effete 
materials, and its sudden arrest by drugs may induce uremic 
convulsions or coma. 

Sudden attacks of profuse watery diarrhea in which the patient 
passes great quantities of liquid from the bowel, with or without 
pain in association therewith, may be due to locomotor ataxia, 
manifesting itself in an "intestinal crisis." 



DIARRHEA 333 

In cases of persistent or obstinate diarrhea, serous or catarrhal, 
in which there is an excessive peristalsis which hurries the intestinal 
contents along so fast that the food cannot be properly digested, 
the physician should remember that fissure of the anus or some other 
source of irritation may be present in the lower bowel which pro- 
duces reflex excitability of the nerves governing the bowel move- 
ments. In other cases a stricture in a feeble, dilated rectum will 
cause retention of feces until irritation, tenesmus, and even loose 
mucous movements are produced. 

If, instead of watery or serous movements, the patient is attacked 
by a more or less acute diarrhea, accompanied by great pain and 
distention of the belly, and if there is marked tenderness on pres- 
sure over the transverse colon and mucus in the feces, which are 
not in very large quantities after the first few movements, there 
is probably present the condition known as colitis, or inflam- 
mation of the colon. It is met with in both children and adults, 
and differs in its course from cholera morbus and cholera infantum 
very markedly. The pain is usually more constant, more aching, 
and less griping in character. Vomiting is not a constant feature, 
as it is in the watery choleraic diarrheas, and the course is more 
subacute, the duration of the illness usually being from one to 
three weeks. If food which is difficult of digestion has been eaten, 
it is passed, still undigested, from the bowel, and is apt to be coated 
with mucus. Such a diarrhea is called lienteric diarrhea. 

Not far removed from this type of cases are those of a more 
chronic character depending upon more grave and lasting altera- 
tions in the gastro-intestinal mucosa. As a rule, the greater part of 
the trouble exists in the colon, and more or less griping pain in the 
neighborhood, namely, in the upper umbilical area and left groin, 
may be present before each movement. The abdomen is apt to be 
distended and quite tender on pressure, particularly in varying 
spots, and considerable loss of bodily weight is apt to ensue, chiefly 
from failure on the part of the digestive tube to absorb the food 
that is eaten. The movements are not markedly watery, but are 
usually unformed and about the consistency of oatmeal gruel or a 
little thicker. Flakes of mucus are often found in large amounts 
in the fecal matter, and the feces may be frothy or flaky, as the 
result of fermentation. Blood and pus are very rarely seen in the 
movements of these cases, unless the blood escapes from an in- 
flamed hemorrhoid. Sometimes, when these cases are very severe 
in character, the mucus takes the shape of long cord-like or worm- 
like strings, or even seems to be membranous in character, the 
so-called mucomembranous colitis. In other instances the feces, 
when formed, are passed in ribbon-shaped masses, due either to 
spasm of the muscular fibres of part of the lower bowel or to cica- 
tricial contractions from the' healing of old ulcerations. In very 



334 THE BOWELS AND FECES 

severe cases the condition of the intestines gradually advances 
from a mild follicular colitis to one of actual deep ulceration, and 
under these circumstances blood and pus may be present in the 
movements. At such times the pain produced by the patient 
having a movement of the bowels, or by the passage of fecal matter 
over the ulcerated surface, may be intense, and the invalid will 
often state that the pain feels as if one spot in the gut were made 
more painful by the feces rubbing over it. Such cases often con- 
tinue for years, while some of them ultimately get well, others 
become chronic invalids from the slow changes in the intestinal 
walls. 

In this connection the diarrhea of tuberculosis is not to be for- 
gotten, depending, as it does, either upon the general infection or 
upon the development of ulcerations in the intestinal canal. 

In some cases in which the patient after exposure to cold or wet 
is seized with violent pain in the epigastrium and a feeling of weight 
in the rectum, a few loose movements and then intense tenesmus 
and bearing-down, with only a few drops of mucus in the way of a 
movement, the condition is one of acute rectal catarrh or proctitis. 

The cases just named in the preceding paragraphs are to be sepa- 
rated from those in which there is true dysentery. Dysentery is a 
term very loosely applied, by the laity in particular, to any form of 
severe diarrhea, particularly if there are blood and mucus in the 
movement. In reality the term dysentery should be limited to 
cases due to an infection. 

Let us suppose that a patient is seized with diarrhea and some 
pain in the belly, and with only a slight chill, or this symptom may 
not be present. The pain soon becomes more and more colicky, 
and the stools are passed with ever-increasing bearing-down or 
tenemus. The effort to empty the bowel, after it is in reality 
thoroughly emptied, results in agonizing bearing-down pains. 
Fever to the extent of from one to three degrees may be present. 
Thirst is excessive, the stomach is usually retentive, and the stools 
are first the ordinary bowel contents, and then mucus, which may 
be blood-streaked. Soon the mucus becomes jelly-like in appearance 
and more thick and tenacious, and, finally, after several days it 
begins to look mucopurulent, and the stools are less frequent. 
Sometimes small, bullet-like, hard pieces of fecal matter are shot 
out of the rectum after severe straining. Recovery usually begins 
at from seven to ten days. The entire trouble seems to be in the 
large bowel, and particularly in the sigmoid flexure and rectum. 
Such are the symptoms of ordinary mild dysentery of hot climates 
or of summer weather in the temperate zone. 

The severity of the disease is much greater in hot weather, 
and the prognosis is not good in severe cases coming on during 
an epidemic. 



DIARRHEA 335 

On the other hand, if the patient has an irregular diarrhea after 
or during a residence in tropical parts, which may or may not have 
a sudden onset, with moderate fever and considerable loss of flesh, 
and has moderate belly-ache, which soon becomes much less, and 
if the stools as just described above become more and more fluid, 
and the diarrhea intermits, the physician should think of the case 
being probably one of so-called amebic dysentery, a condition of 
infection by the so-called amebae coli. The course of the disease 
is slow, lasting from six to twelve weeks, and the death rate is high. 
Convalescence is always very slow, and liver abscess due to an 
hepatic infection by the amebae coli is very frequent. Sometimes 
secondary abscess of the lung develops. 

A positive diagnosis of this variety of dysentery is made by the 
discovery of the amebae in stools. These microorganisms possess 
active ameboid movements and are found in greater number when 
the diarrhea is severe. They are to be sought for in the small 
gelatinous masses which are found in the feces. Sometimes the 
entire stool seems loaded with amebae; at other times only a most 
careful search will discover them. They are more refractive than 
the cells found in the feces, and contain numerous vacuoles, so 
numerous in some cases that the cells look very granular. These 
must not be mistaken for the compound granular bodies found in 
the feces. When they are active a division into an endosarc and 
an ectosarc can be discovered. Often red blood cells will be found 
in the amebae. 

Epidemic dysentery is usually due to Shiga's bacillus. 

Sometimes a diphtheritic or pseudomembranous dysentery is 
developed in persons having chronic heart disease, and it has been 
seen as a sequel of acute croupous pneumonia. This is called 
secondary diphtheritic dysentery, and death generally results from 
exhaustion, only a suspicion of the intestinal condition having 
existed during life. Such a state is sometimes a complication of 
Bright's disease, probably owing to the irritation of the intestinal 
mucous membrane produced by the urea decomposing into the 
carbonate of ammonium. In acute primary dysentery of a diph- 
theritic character the patient may rapidly pass into a typhoid state, 
and the case be diagnosticated as one of typhoid fever with profuse 
diarrhea. The discharges are valuable means of separating the 
two conditions (enteric fever and diphtheritic dysentery), as they 
often are filled with blood and mucus in dysentery, a condition 
rarely seen in typhoid fever. 

Dysentery may be confused with the diarrhea sometimes pro- 
duced by a malignant and ulcerating growth in the sigmoid flexure 
or rectum, but a physical examination will usually reveal the tumor, 
and the cachexia will aid in pointing to it as the cause. Syphilitic 
ulceration of these parts may cause a somewhat similar train oi 
symptoms. 



336 THE BOWELS AND FECES 

Again, it is by no means rare to meet with the passage of several 
mucopurulent movements each day in persons who have pulmon- 
ary gangrene or pulmonary tuberculosis, due to the swallowing of 
fetid sputum and the production of tuberculous ulceration of the 
bowels. 

Diarrhea is also a symptom of septicemia. Distantly allied to 
this form of diarrhea is that seen in persons who have dissected a 
putrid body (" dissecting-room diarrhea," so called.) 

Finally, it is interesting to note that paroxysmal attacks of sero- 
mucous or bloody diarrhea sometimes come on in cases of exoph- 
thalmic goitre. Diarrhea of a more or less severe type may come on 
in cases of hysteria, often associated with tremendous eructations 
of gas and rumbling in the stomach and bowels. 

Fatty diarrhea may ensue if feeble persons already suffering from 
irritable bowels take an excess of cod-liver oil, and in some cases it 
possesses great diagnostic importance. If associated with glyco- 
suria, it gives us reason to believe that there is disease of the 
pancreas producing both the glycosuria and the lack of digestion 
of the fats. Sometimes in jaundice, however, fat is found in the 
stools owing to the lack of bile to emulsify it in the intestine. 

The Feces. — In this connection we naturally pass on to a discus- 
sion of the diagnostic indications of the feces. In the first place, it 
must be remembered that the quantity of the feces depends upon 
the quantity of the food, and again that the quantity varies with 
the character of the food, for if the food be such as to be bulky, yet 
contains little nutritive material, there will be a large residue to be 
passed out as feces; whereas if the food be almost entirely com- 
posed of materials which can be assimilated, very little residue is 
left, and the feces are consequently small in bulk. Thus, the 
cow eats a large bulk of food and passes large amounts of fecal 
matter, while the dog eats meat and passes very small amounts. 

Again, it is not to be forgotten that manyjoods actually increase 
intestinal peristalsis, and so produce large and loose movements, 
as oatmeal and wheaten grits or apples, while other foods, such as 
cheese, do the opposite. If the stools are large and copious and the 
food which the patient has taken is not of a kind leaving a large 
residue in the bowel, the indication is that there is non-absorption 
of nutritive materials, with probable wasting of the patient. 

The consistency of the feces in health varies from a formed 
" stool" to a mushy condition; but in disease we have a liquid watery 
stool if the trouble be serous diarrhea, and a pasty or slimy stool 
if it be due to a catarrhal state of the bowels. The passage of hard 
scybalous masses mixed with liquid indicates that the feces have 
become dried and hard in the sacculations of the colon, and are 
passed only when they cause so much irritation as to produce 
diarrhea. If the feces are in narrow bands or flattened ribbon- 



THE FECES 337 

shapes, there is probably a stricture of the rectum, offering an 
obstruction to their passage. A mushy or semiwatery "pea- 
soup" stool is often seen in typhoid fever. 

The odor of the stools depends very largely upon the food which 
is taken and upon the degree of putrefaction or fermentation 
present in the bowels. In nursing children the stools often have a 
faintly sour odor, and in the diarrhea of nurslings with acid fer- 
mentation there is an odor of the fatty acids. If the process is 
marked, this odor becomes actually foul, and in cholera infantum 
the stools have a musty, mousy odor. If malignant growth of the 
bowel is present, the odor is fetid, as it is also in gangrene of the 
intestine. 

The color of the stools is of great diagnostic importance in several 
conditions. In health the feces should be brown or brownish black, 
the color being partly due to the food, but chiefly to the bile (hydro- 
bilirubin). Certain fruits render the stools dark in color, and some 
drugs, such as iron and bismuth, make them black, and hema- 
toxylon often makes them look red. 

In the stools of persons living on a pure milk diet we usually 
find little color comparatively. Again, in cases of jaundice, phos- 
phorus poisoning, and acute yellow atrophy of the liver, the stools 
are very light in color, owing to their lack of biliary coloring. 
They are also apt to be very light in chronic lead poisoning. 

Bilious stools are either golden yellow, greenish, or reddish in 
hue, and if the flow of bile is profuse, they are apt to be watery. 
Greenish stools looking as if they contained chopped spinach are, 
however, a peculiarity of the diarrhea of fermentation, particularly 
in infants, the color being due to color-forming microorganisms; 
but a greenish stool may also be produced in an infant by the 
persistent administration of sodium bicarbonate. 

If the stools are well mixed with mucus, the catarrhal process 
probably exists in the ileum; but if they consist of hard masses of 
feces coated with mucus, the disease is probably a colitis. 

Bloody stools are most commonly due to hemorrhoids which are 
eroded. The blood may be bright if the hemorrhoid be a small 
arterial bunch, or more dark and grumous if slow oozing has gone 
on for some time prior to the movement. As a rule, the brighter 
the blood in the stool the nearer its source is to the anus, and the 
darker the blood the higher is its source in the bowel. Thus, if 
the stools are tarry-looking, the blood is almost certainly from the 
small intestine, and probably arises from a duodenal or other ulcer 
or from carcinoma of the stomach or bowel; while if it is only 
somewhat changed in appearance, it may be due to an ulcer or 
ulcerated morbid growth in the colon. Sometimes, however, when 
the hemorrhage from the ileum is very profuse, as in typhoid fever. 
the blood comes from the anus only slightly changed in appearance. 



338 THE BOWELS AND FECES 

Stools containing pus may receive this material from the surfaces 
of ulcers, but usually the source of the purulent matter, if it is 
present in large amount, is an abscess which has ruptured into the 
bowel, as, for example, in perirectal, or even subphrenic abscess. 

Finally, we may nnd gall-stones in the stools, which, if they are 
passed soon after their escape into the bowel, are found to be 
faceted. Stools which are being searched for gall-stones should be 
washed through a sieve in such a way as to catch the stone and let 
the fecal matter through. The intrahepatic gall-stone is not faceted 
and crumbles easily. This stone rarely escapes, because it is 
embedded, and if it does get into the bowel is usually broken up. 
All stones or concretions found in the feces are not to be considered 
as gall-stones. They may be pancreatic calculi in rare instances, 
or they may be fecal stones (coproliths) or intestinal stones (entero- 
liths). Fecal stones are simply hard inspissated masses of feces, 
which may attain a very large size, whereas intestinal stones are 
composed of heavy, brown concentric layers of phosphates of 
calcium and magnesium around some nidus, as a seed or piece of 
bone. Sometimes they are concretions of insoluble drugs, such as 
salol or magnesium carbonate. 

Intestinal sand appears to be a characteristic symptom of certain 
types of neurasthenia which is often provocative simultaneously 
of mucomembranous colitis. The chief constituent of intestinal 
sand is said to be calcium sulphate. Care must be taken to 
separate true intestinal sand from small seeds or the small sand-like 
bodies found about the seed core of pears. 

Very rarely a portion of the bowel sloughs away, and yet recovery 
takes place. This is seen sometimes in intussusception. 



INTESTINAL PARASITES. 

Aside from the character of the stools themselves, we often 
search for the cause of an ailment in the passages, either for foreign 
bodies, such as pebbles or pins, or for intestinal parasites (worms). 
Sometimes worms may exist for long periods of time in the bowel 
without causing any symptoms, and, again, in children in par- 
ticular, they may cause great systemic disturbance by producing 
disorder of the digestion or reflex irritation. 

Under the name of tape-worm or cestodes we find in the intestine, 
and often in the stools, a parasite occurring in segments which are 
flat and ribbon-like, and usually from a quarter to one-half inch in 
length. The worm itself may be several yards long. Its head is 
small, and it maintains its hold on the bowel by its head. The seg- 
ments are usually broken off one by one or in chains, and escape 



INTESTINAL PARASITES 



339 



in the stools, and the stools also contain the ova or eggs of the 
parasite, which are developed in each segment, which also possesses 
male and female organs. 




Fig. 126. — Ascaris lumbricoides dis- 
sected and walls thrown back. a. 
Genital orifice, b. Intestine, c. Ovi- 
ducts, d. Longitudinal band. e. 
Ovaries. (Heller.) 



Fig. 127. — Oxyuris vermicularis 
magnified, a. Young female, b. 
Male. c. Mature female, full of eggs. 
(Payne.) 



34° 



THE BOWELS AND FECES 



According to the shape of the head and the size of the worm 
and the source of infection, we divide tape- worms into three classes: 
the Tenia solium, the Tenia mediocanellata, and the Bothrio- 
cephalus latus. 




Fig. 128. — Trichocephalus dispar, natural size. a. Female, b. Male. (Payne.) 



a b 
Fig. 129.— Ankylostomum duodenale magnified. 

(Bristowe.) 



a. Male. b. Female. 



If the patient passes a worm of from one to three yards in length, 
the head of which is about the size of a pin-head and glistening 
gray in appearance, the rest of the worm being yellowish white, 
and if upon the head can be seen four pigmented suckers surrounded 



INTESTINAL PARASITES 



341 



by a crown of hooks, that worm is a Tenia solium, and is probably 
derived by the patient from raw or uncooked pork. The eggs of 
the Tenia solium must be sought for by a microscope. They are 
round and covered by a hard shell, which upon pressure breaks 
into small fragments. In the shells may be found a few hooklets. 
These eggs are passed out in the feces by the host, and are then 
swallowed by the pig, into whose muscles the hooklets migrate and 
form cysts. In these cysts the hooklets develop, and when a man 
eats the meat raw they enter his intestine, attach themselves, and 
from them a tape- worm is developed. 




Fig. 130. — Ova and embryo of Uncinaria americana. a, unicellular ovum; 

b, c, d, e, ova showing various stages of segmentation; /, g, ova containing larval 
uncinariae; h, peculiarly shaped ovum; i, larval worm just emerged from shell; 

c, larva extended after emergence. (Stiles.) 



If the worm is from four to five yards long and the segments after 
leaving the anus have motile power, and if the head is larger than 
that of Tenia solium and devoid of hooklets about the suckers on its 
head, it is probably the Tenia mediocanellata or saginata. The egg 
is slightly larger that that of the solium. This worm usually comes 
from eating raw beef. The Bothriocephalus latus is the largest of all 
tape-worms, often reaching seven to eight yards in length. It has 
a long head with two long, narrow suckers. The eggs are oval, very 
large, and the shell is light brown in color, and very easily broken. 
This parasite is not common in America, but is a very frequent 
cause of profound anemia in the persons whom it infects. Its joints 
are only rarely thrown off, so its presence is often overlooked, and 



342 THE BOWELS AND FECES 

this renders the search for the eggs very important in severe 
anemia with no ascribable cause. This worm is usually derived 
from fish. A worm which is comparatively rare is the Tenia 
cucumerina, which has a head with sixty hooks. It infects dogs, 
cats, and sometimes children. 

A round-worm, looking like an ordinary earth-worm, appears 
sometimes in the stools, and is called Ascaris lumbricoides . It is 
sometimes vomited, and rarely causes trouble by crawling into 
and blocking the common biliary duct. 

Fine thread-like worms inhabiting the rectum are the Oxyuris 
vermicularis. 

A very important diagnostic find in the feces is a worm looking 
very much like the thread-worm, but somewhat larger, which 
inhabits the duodenum. It occurs as the Ankylostomum duodenale, 
sometimes called the Uncinaria duodenale and as the Uncinaria 
americana or Necator americana. These parasites belong to the 
nematodes. The Ankylostomum duodenale is possessed of two 
pairs of hook-shaped ventral teeth and one pair of dorsal teeth 
projected forward. The male parasite is 8 to 10 mm. long, and 
the female is from 10 to 18 mm. long. The Uncinaria americana 
has no hook teeth but a ventral pair of slightly developed lips 
and a dorsal pair of semilunar plates or lips. The male is 7 to 
9 mm. long and the female 9 to 11 mm. long. The eggs are elipsoid 
and contains a well-developed embryo or are segmented. If the 
stools are set aside in a warm place the embryos can be seen to 
develop under the microscope if a small part is spread on a slide. 
The worms themselves are often O of a red hue. A rough test proposed 
by Stiles is to place a small part of the stool on white blotting paper 
for an hour. If it is now removed and the paper is stained red the 
worm is present. The importance of finding this parasite lies in 
the fact that it produces the most profound and acute anemia 
by sucking blood from the intestinal wall, although some assert 
that the anemia is not due to loss of blood but to a poison formed 
by the parasite. The worms are usually only found after a 
vermifuge is taken, but the eggs are always present in the feces 
as unsymmetrical, thickly covered, segmented globules. 

The so-called whip-worm, or Trichocephalus dispar, is a fine 
thread-worm without any medical interest. 



CHAPTER XII. 
THE URINARY BLADDER AND THE URINE. 

Disorders and diseases of the urinary bladder — Retention of urine — Incon- 
tinence of urine — The characteristics of normal and abnormal urine. 

THE BLADDER. 

The objective symptoms of bladder difficulties are generally local, 
unless they are very chronic, when the face may appear worn 
and weary, and, if a purulent cystitis be present, septic fever 
may occur. The subjective symptoms are tenderness, tenesmus, 
pain (see chapters on Pain and on the Abdomen), and retention or 
incontinence of urine. 

Retention and Incontinence of Urine. — Retention and incontinence 
of urine usually depend upon causes arising outside this viscus, 
such as an enlarged prostate or a stricture. They may arise from 
disease or injury which destroys or temporarily impairs the func- 
tion of the cells in the spinal cord which govern the contraction 
of the muscles involved in expelling urine from the bladder. These 
centres are situated at or about the level at which are given off 
the second, third, and fourth sacral nerves. (See pages 93 and 94.) 

Paralysis of the bladder with retention may, therefore, follow 
severe injuries to the spinal cord, produced by a fall, blows, or other 
traumatisms, or be due to a myelitis which destroys such centres. 
(See chapter on the Legs and Feet, part on Paraplegia.) The 
bladder symptoms seen in myelitis — transverse, traumatic, or 
otherwise — usually come on in the acute form within a few hours 
after the sensory and motor disturbances have been noticed by 
the patient, and either incontinence or retention, or retention 
incontinence, may occur. 

If, however, the myelitis is not complete, the bladder may escape. 
On the other hand, if the portion of the cord which is involved 
happens to be that part governing the bladder, vesical symptoms 
may develop before the motor symptoms are clearly marked. 
Again, it is a noteworthy fact that when recovery takes place 
vesical control may be regained before any marked improvement 
can be found elsewhere. Often the loss of control of the bladder is 
such that the patient cannot voluntarily expel the urine and cannot 
retain it, and it dribbles away without his knowledge. Under such 



344 THE URINARY BLADDER AND THE URINE 

circumstances there is probably a myelitis involving the lower part 
of the dorsal cord and the upper and lower parts of the lumbar 
cord; in other words, all that portion in which the vesical centres 
are situated. If the dribbling of urine takes place without dis- 
tention of the bladder, the fluid passing directly from the ureters 
through the urethra, the lower part of the lumbar enlargement of 
the cord is affected, owing to paralysis of the sphincter. On the 
other hand, distention of the bladder, due to retention of urine, 
occurs when the myelitis is in the lower dorsal and upper lumbar 
cord, and is due to paralysis of the detrusor muscles, which make no 
effort to expel the urine, while the sphincter, the centres of which 
are intact, maintains a tightly closed orifice. Such cases may 
empty the bladder spasmodically at long intervals (overflow 
incontinence) — that is, sphincter paralysis from distention may 
ensue. In such a condition the bladder should be emptied by the 
catheter to avoid paralysis and vesical disease. To put the case 
in another way, we can say that the spinal centre for the control 
of the walls of the bladder is situated at a higher point in the cord 
than is that for control of the sphincter, and, therefore, retention 
of urine indicates a lesion higher up in the cord than does incon- 
tinence without retention. Precisely similar vesical symptoms 
occur in cases of spinal tumor producing transverse lesions of the 
cord (see chapter on the Feet and Legs, Paraplegia), or may arise 
from spinal apoplexy. 

The bladder symptoms of locomotor ataxia are often quite char- 
acteristic, and are to be separated from those of myelitis, spinal 
tumor, and the vesical troubles due to traumatisms of the cord. 
The disorder depends entirely upon interference with the reflexes of 
the viscus, and so presents varying symptoms which are motor and 
sensory. The patient sometimes complains of the fact that he has 
to strain for a long time before he can start a stream, which, even 
after it is started, is often jerking or interrupted; or, again, he must 
sit down and bend over in order to have the aid of his abdominal 
muscles before he can evacuate the bladder. As a result of this, 
residual urine in excess is always present, and cystitis or milder 
degrees of vesical irritability develop. In other instances the desire 
to urinate comes upon the patient so suddenly and forcibly that the 
urine is voided before he can, with his impaired gait, reach a place 
to pass it in a proper manner; on the other hand, it may be retained 
and can only be removed by a catheter. Still others find that 
urine escapes on laughing, coughing, or sneezing, owing to lack of 
complete control of the bladder and its sphincter; or, again, after 
many attempts to urinate, the patient gives up the effort, only to 
be humiliated by an involuntary passage of urine immediately 
after his penis has been withdrawn into his clothes. 

These symptoms differ so materially from those present in 



THE BLADDER 345 

myelitis as to make a diagnosis as to their cause nearly always 
possible. 

In obscure cases of ataxia the vesical symptoms may aid the 
diagnosis quite markedly; thus the presence of bladder symptoms 
would confirm a diagnosis of ataxia as against pseudotabes due to 
peripheral neuritis. Again, in myelitis the presence of vesical 
symptoms points to that disease, and excludes from the diagnosis 
such affections as poliomyelitis and lateral sclerosis, affections in 
which vesical paralysis rarely, if ever, occurs. Precisely similar 
vesical symptoms are sometimes seen in cases of general paralysis 
of the insane, but the delusions of grandeur or of persecution and 
other characteristic signs of this disease separate it at once from 
ataxia. 

Retention sometimes comes on in locomotor ataxia, in which 
disease the impulses from the bladder are not recognized, or are 
perverted, so that the sphincter which closes the bladder does not 
relax to permit the escape of urine, or the cord or brain fails to 
recognize that the bladder is full, and so sends no impulse for its 
relief. Again, retention of urine may arise from paralysis of the 
muscular part of the vesical walls by pressure produced in severe 
labor (child-birth). 

Finally, we see cases in which the bladder cannot be emptied, 
because its walls have been paralyzed by overdistention with 
urine. 

Incontinence results from loss of power in the sphincter, due 
to injury or disease in the cord at the level of the second, third, 
and fourth sacral nerves; and this, is a far more frequent 
occurrence than is absolute retention. The real condition under 
these circumstances is that the expelling muscles and retention 
muscles are both paralyzed, so that the urine accumulates in 
the bladder and then dribbles through the unguarded neck of the 
bladder. Sometimes, too, this incontinence is caused by the 
urethra being so insensitive that it fails to recognize the presence 
of the urine, and so does not send an impulse to the sphincter to 
tighten its hold. Incontinence also results from excessive reflex 
irritability of the walls of the bladder, so that the urine no sooner 
trickles into this viscus than an impulse is sent to the spinal centres 
which send a motor impulse to the muscles of expulsion. This is 
often the condition in the nocturnal incontinence of children, for 
as soon as the child sleeps its will-power over the bladder ceases. 
and reflex activity is alone in control. Irritating, concentrated 
urine may pervert the reflexes of the bladder and so cause incon- 
tinence. 

Sensory Disorders. — The sensory disturbances of the bladder will 
be found discussed in the chapter on Pain, but it is worth noting 
here that accompanying the symptoms already named as charac- 



346 THE URINARY BLADDER AND THE URINE 

teristic of locomotor ataxia vesical crises of spasm and pain fre- 
quently occur. 

When there is pain in the bladder, made worse by the attempted 
act of micturition, and tenesmus, with pain darting into the 
urethra, there is probably present a cystitis; but the physician 
should remember that cystitis may be present with almost no 
painful manifestations, even when in its acute form. In other 
cases this condition arises from concentration of urine, which 
produces irritation of the viscus. In children this concentration 
of the urine is the most common cause of nocturnal urinary in- 
continence. 

Involuntary passage of the urine sometimes occurs in idiots, in 
some cases of insanity, in attacks of apoplexy, or any condition of 
abnormal unconsciousness, and sometimes in very severe infectious 
diseases, such, for example, as diphtheria. Oftentimes it results 
in children from irritation of the foreskin or vagina, or from rectal 
irritation produced by seat-worms, since all these causes disturb 
the reflex activity of the spinal centres. 

Obstruction to Urinary Flow. — Interference with the passage 
of urine may also arise from two causes which are surgical in 
character, namely, stone in the bladder and tumors of the bladder, 
which are often situated near its neck and so produce obstruction. 
Finally, in old men, that most commonly met with cause of difficult 
micturition, enlargement of the prostrate, is to be remembered. 

Aside from these causes of interference with the passage of 
urine, we must not forget the possibility of its obstruction by 
stricture of the urethra, nor should the physician ignore the fact 
that some persons have "nervous bladders," which will not re- 
spond to an effort of the will if another person is near by, although 
the urine is at once passed as soon as the patient is alone. 

THE URINE. 

Changes from the normal in the urine, as already stated, are 
determined, first, by its general appearance, quantity, odor, 
specific gravity; second, by its microscopic appearance; and, 
third, by its chemical reaction and responses to tests. Any changes 
in this fluid of an abnormal character are solely symptomatic, 
and point with more or less distinctness to disorders of bodily 
metabolism, disease or disorder of the kidneys, ureters, bladder, 
or urethra, and sometimes of the prostrate, testicles, vagina, or 
uterus. 

The urinary secretion is one which is too frequently ignored by 
the student and physician in studying the diagnosis of disease. 
In many instances it will, if properly tested, give such positive 
evidence in regard to obscure affections that a correct diagnosis 



THE URINE 347 

is at once possible, and in other cases its examination, as a matter 
of routine, will discover important facts, the existence of which has 
been unsuspected. Again and again will a diagnosis prove erro- 
neous if the importance of urinary examinations is ignored, and 
costly errors for the patient and the reputation of the physician 
ensue. 

In asking questions about the character of the urine passed and 
its quantity, the physician should be sure that the patient clearly 
understands his question. Often he is told that much urine is 
passed, when, in reality, it is really in small amount, but passed 
often; or that it is blood red, when red because of the presence 
of high-colored urates. In inquiring about its color, we should 
remember that if large amounts of liquid have been swallowed it 
will probably be light in hue, or if small amounts of drink are 
taken, dark in hue. So, too, active exercise in warm weather 
may produce 'a somewhat concentrated urine, because much liquid 
has been lost by the skin in sweat, and the muscular exertion 
produces large quantities of nitrogenous material indicative of 
tissue waste. In winter the urinary flow is more apt to be copious 
because the skin is inactive. 

The urine which is to be tested should always be passed directly 
into the vessel in which it is brought to the physician, and this 
bottle should be scrupulously clean; or, if the urine is passed 
into any other vessel, care must be taken that it is perfectly clean. 
When it is thought that urethral disease may obscure the investi- 
gation a catheter should be passed, all urine in the bladder drawn 
off, and then the catheter allowed to remain in place, so that the 
urine will trickle directly from the ureters to the catheter, and so 
to a receiving vessel. This is very important when the urine is 
voided involuntarily. If the condition of the bladder is bad, 
this viscus should be washed out by boric acid injections, in 
order to prevent it from contaminating the urine which is to be 
tested or ureteral catheterization be practised. 

Quantity of Urine. — The quantity of urine passed by a healthy 
adult varies from two to four pints in the twenty-four hours, 
according to the amount of liquid ingested, the freedom of per- 
spiration, and the amount of exercise. 

The significance of any great and constant increase in the 
amount of urine passed in a given case is various. Thus, we 
find it greatly increased in diabetes mellitus, in diabetes insipidus, 
in some cases of neurasthenia, and in some cases of hysteria. It 
is also increased in many cerebral lesions. High blood-pressure, 
particularly if associated with chronic contracted kidney, causes an 
increase in the urine; and, therefore, if a patient has to urinate 
frequently or has to arise at night to empty a full bladder, we 
suspect this trouble if diabetes and cystitis are excluded. 



348 THE URINARY BLADDER AND THE URINE 

A copious flow of urine of a low specific gravity and of a pale, 
clear appearance, containing fatty, hyaline, and finely granular 
casts, is often seen in cases of amyloid disease of the kidney, and 
the presence of syphilis, of prolonged suppuration, or extensive 
bone disease, due, it may be, to tuberculosis, with concomitant 
enlargement of the liver and spleen, separates this condition from 
any other ailment. Albuminuria may be a marked symptom or 
be entirely absent. 

Polyuria also ensues if the heart and kidneys are stimulated to 
increased effort by the action of drugs, such as digitalis, caffeine, 
or alcohol. We also find an increase in urinary secretion, without 
its possessing any grave significance, in convalescence from such 
diseases as typhoid fever and pneumonia. 

The quantity of the urine is diminished in cases in which the 
heart fails to do its proper amount of work, with resulting stasis 
of the blood in the kidneys, and whenever any large amount of 
liquid is taken away from the body, as in diarrhea. It is also 
decreased by fevers and by the sweats following febrile movement. 
Persistent vomiting also has a similar effect. Parenchymatous 
nephritis, both acute and chronic, greatly diminishes the urine, 
and in grave, fatal illnesses urinary suppression may occur. 

The Odor. — The odor of freshly passed urine is faint, but char- 
acteristic. What is often called a " urine odor" is really due to 
the development of ammonia in urine which has decomposed. 
The odor is altered by many drugs and foods, notably by copaiba, 
turpentine, eucalyptus, valerian, musk, asafetida, and by as- 
paragus. Diabetic urine possesses a heavy, sweet odor. 

The Color. — The naked-eye examination of the urine often gives 
very important information, if its clearness, opacity, and color 
are observed. Its clearness and color are modified by the presence 
of pigments derived from outside sources, such as the educts of 
carbolic acid or salicylic acid, of senna or hematoxylon; and from 
urobilin, and many other substances coming from inside sources, 
such as blood and bile. (See below.) Many of these causes may 
render it opaque, but there are two conditions, above all others, 
which make the urine cloudy even when freshly passed, namely, 
cystitis with phosphaturia and chyluria. A urine which becomes 
cloudy after it becomes cold usually contains an excess of phos- 
phates. After urine has stood for some hours it often becomes 
opaque, because it has undergone decomposition changes. 

A black urine is sometimes seen in cases of melanotic sarcoma, 
ochronosis, and alkaptonuria, or it may turn black after the 
brownish urine produced by carbolic acid or uva ursi has been 
exposed to the air by reason of the presence of hydroquinone. 

Hematuria. — If the color be due to blood or hematuria, the 
urine will be of a more or less bright red, according to the fresh- 



THE URINE 349 

ness of the sample brought to the physician and the seat of the 
hemorrhage. If the urine has been voided several hours, it will 
be of a dingy red or smoky hue, and on standing will deposit 
a coffee-ground or reddish sediment of a somewhat flocculent 
appearance. If, on the other hand, the urine is seen as soon as 
passed, it may be a bright red or a dingy red, according to the 
seat of the hemorrhage and the time which has elapsed since 
the bleeding began; if it has arisen in the kidney or ureter or 
bladder, and has been gradual, the mixture of blood and urine 
will be so intimate that changes in the blood will have taken place, 
whereas if the hemorrhage has occurred, simultaneously with 
urination, from the neck of the bladder or the urethra, the blood 
will be almost unchanged when it escapes from the urethra. The 
presence of clots in recently passed urine indicates a not very 
recent hemorrhage, and yet one of such size that the urine could 
not by dilution completely prevent clotting. 

When the blood comes from the kidney some of the possible 
causes 'are acute parenchymatous nephritis, resulting from any 
one of the severe infectious diseases, such as scarlet fever 
or malarial fever; embolism, resulting from ulcerative or other 
forms of endocarditis, producing renal infarction; sepsis of the 
kidney, the ingestion of irritating drugs, such as cantharides or 
turpentine; and injuries of the back, producing rupture or other 
disorganization of the kidney. AH these conditions produce what 
may be called acute hematuria. If the cause be acute nephritis 
due to an infectious malady, such as scarlet fever, the presence 
or history of an eruption, and the presence of casts in the urine 
clears the diagnosis. 

Hematuria due to malarial poisoning may appear with the first 
malarial paroxysm, of the intermittent type, which the patient 
has ever had, and at a time when the history of the case renders 
it certain than an old malarial condition could not have previously 
damaged the renal tissues or those of other organs in the body. 
In other words, there are cases in which a free hemorrhage from 
the kidney takes place, by reason of the chill, in much the same 
manner in which hemorrhage takes place in acute nephritis due 
to exposure to cold or to irritants. Under these circumstances 
there may or may not be developed a true organic lesion of the 
kidney in the sense of permanent disease. 

Secondly, we have cases in which bloody urine appears, not in 
the first malarial paroxysm of the intermittent type, but with the 
later attacks, which may have followed the first either rapidly or 
slowly. In these cases there may be no further cause for the 
hemorrhage than excessive congestion, but the vast majority of 
such patients present distinct renal changes, which permit such a 
symptom to develop when the paroxysm asserts itself. 



350 THE URINARY BLADDER AND THE URINE 

Thirdly, we pass from those cases of bloody urine due to 
intermittent forms to those due to remittent attack. In these 
patients the process by which a bloody colored urine is developed 
may be very complicated, since it may be due to renal disease, 
functional or organic, or to a true hemoglobinuria, arising from 
dissolution of the red blood cells in the bloodvessels or blood- 
making organs. 

Finally, there is a type of malarial hematuria which is brought 
on by the administration of quinine (Karamitsas and others.) 

All these forms of hematuria can be diagnosticated by the 
presence of the malarial parasite in the blood and the character- 
istic malarial symptoms, except that which occurs in persons who 
have a dyscrasia from old malarial poisoning when no organisms 
are found. 

If the hematuria be due to embolic infarction of the kidney, an 
examination of the heart will probably reveal signs of valvular 
disease, from which source the embolus will have resulted, or in 
other cases the physical signs, combined with the history, will 
show malignant endocarditis with renal sepsis therefrom. Some- 
times thrombosis of a renal vein occurs in feeble, wasted infants, 
and so causes hematuria. If embolism is not the cause of the 
hematuria, the history of the ingestion of an irritating drug will 
be the diagnostic guide, or, if injuries be the cause, a history 
of trauma will elucidate the case. 

The causes of chronic or persistent hemorrhage from the kidney 
are chronic diffuse nephritis, cancer of the kidney, calculus in the 
pelvis of the kidney producing ulceration, injury of the kidney by 
jarring of a stone, tuberculosis of the kidney, the most common 
cause, and cystic degeneration. It is often an early symptom of 
hypernephroma . 

If the chronic hematuria arise from chronic diffuse nephritis, 
which is rarely the case, the diagnosis may be aided by pallor 
of the skin, anorexia, nausea, headache, decreased amount of 
urine, and albuminuria. The cause of the nephritis and the source 
of the bleeding demands careful investigation in such cases. It 
has been pointed out by Chute and others that it is quite possible 
for an acute infection to involve only one kidney or only part 
of one kidney, whereas a toxic nephritis due to a systemic poison 
naturally involves both kidneys. The history of the case and the 
use of the cystoscope, or the ureteral catheter, will determine 
whether the blood comes from one kidney, and if this be the case 
and the bleeding is excessive a nephrectomy may be needful to 
save life. On the other hand, if the history is one which indicates 
a toxic nephritis, in which state both the kidneys are probably 
affected, and if it is found that the blood comes from both kidneys, 
then nephrectomy is contraindicated, since the remaining kidney 



THE URINE 351 

would be unable to maintain life and the hemorrhage would not 
be arrested. A bacteriological examination of the urine from one 
ureter which reveals infection, while the urine from the other 
ureter is sterile, may also aid the diagnosis. 

If the cause be renal cancer, the cachexia, pain, and the mixture 
of pus, blood, and disorganized renal tissue in the urine will render 
the diagnosis possible. If due to calculus, there may be a previous 
history of attacks of renal colic or of violent pain in the kidney; 
and if ulceration of the renal pelvis has occurred, there will be 
disturbances of the body temperature, pain in the lumbar area, 
and pus in the urine. The presence of tubercle bacilli in the 
urine decides the presence of renal tuberculosis, but unfortunately 
the bacillus is often not found. If cystic degeneration is present, it 
can only be determined when the cyst is large enough to be felt. 
A sudden profuse hemorrhage in the urine, sufficiently large to 
endanger life, may come from such a cystic tumor of the kidney. 
In all these instances an x-ray examination may give valuable 
results. 

Blood from the kidney usually possesses the following character- 
istics: it is well mixed with the urine, and is generally altered in 
appearance, to the naked eye and under the microscope, both as 
to color and the shape of the corpuscles which may appear as 
the pale, almost invisible bodies known as " shadow corpuscles.'' 
The cells and casts which may be present are changed in color 
by the hemoglobin which is free in the urine. Again, blood casts, 
or red blood corpuscles clinging to casts, indicate renal hemor- 
rhage. When the blood comes from the pelvis of the kidney it 
may appear in the urine in long, worm-like clots (moulds of the 
ureter), and their extrusion from the ureter produces symptoms 
of colic. Under such circumstances there may be alternations of 
hematuria and normal urine, due to the blocking of the ureter on 
the diseased side by a clot, so that all the voided urine comes 
from the healthy kidney. 

Blood in the urine may arise from the bladder walls and be due 
to an acute cystitis, to papilloma, malignant growth, or tuber- 
culosis of this viscus, or to injury. These vesical causes should, 
if possible, be determined by the use of the cystoscope. 

It must not be forgotten also that blood in the urine may be due 
to menstrual discharge, to blood from uterine fibroids or malignant 
uterine ulceration, and that it is possible for a malingerer to place 
blood in the urine, with the object of deception. Rarely in certain 
cases of locomotor ataxia, hematuria develops after the vesical 
crises which have already been described (see Bladder in this 
chapter). This is due to capillary hemorrhage from the bladder 
walls. 

There are other varieties of hematuria which must not be for- 
gotten, although comparatively rare, namely, that due to the 



352 THE URINARY BLADDER AND THE URINE 

presence in the blood of the Filaria sanguinis hominis, which is a 
condition in which the presence of chyle in the urine so masks that 
of the blood that the urine has the appearance of pinkish cream 
or milk, but microscopic examinations will show blood corpuscles 
and fat globules, as well as the embryos of the filaria. (See 
Chyluria in this chapter.) Another still more rare cause of hema- 
turia is the Distoma hematobium of Egypt and Abyssinia. This 
produces what has been called tropical hematuria. The third 
cause is eYen more rare in man, namely, the Strongylus gigas, 
which also causes pyelitis and renal colic. A fourth form of 
hematuria is that seen in some cases of scurvy, particularly of 
the infantile type, and, lastly, hematuria may also appear as a 
symptom of purpura hemorrhagica, hemophilia, and very rarely in 
leukemia. 

Hemoglobinuria. — The urine, when not discolored by blood, 
may be discolored by the presence of the coloring matter of the 
blood. This is called hemoglobinuria. 

Hemoglobinuria arises from a number of causes, such as infec- 
tious disease, poisoning by mushrooms, and excessive doses of 
certain coal-tar derivatives, or of chlorate of potassium, or glycerin. 
Malarial poisoning sometimes causes it instead of hematuria. One 
form of malarial hemoglobinuria is intermittent, the urine being 
at one hour limpid, the next hour bloody, and the third hour 
again clear. Probably many cases of so-called malarial hemo- 
globinuria are due to another parasite not as yet isolated. 

The possibility of confusing paroxysmal hemoglobinuria, when 
in a severe form, with that due to severe malarial infection, is 
very great, for the history of paroxysmal hemoglobinuria teems 
with reports of cases in which the chief manifestations of a 
malarial attack were present, such as chills, fever, and sweats. 
Paroxysmal hemoglobinuria is a condition which seems to be pro- 
duced by mere chilling of the surface of the body or even by 
immersing the hands of a susceptible person in iced water. It 
may also be produced either by exposure to cold and damp or to 
the chill of the milder forms of malarial paroxysm. Hemoglobinuria 
may also be a symptom of that curious vasomotor affection called 
Raynaud 9 s disease. 

Microscopic examination of the urine in such cases will show 
no corpuscles, although the urine will be coagulated by the nitric- 
acid test; but the coagulum does not settle in flakes, as it usually 
does in albuminous urine, but floats on the surface in a brownish 
mass. The naked-eye appearance of the urine is that of clear port 
wine. If a few drops of this urine be placed on a watch-glass 
and a drop of strong acetic acid be added, the blood crystals of 
Teichmann will be found by the aid of the microscope, showing 
that the coloring matter is hemoglobin. 



THE URINE 



353 



The following table, based on Purdy's well-known work on 
Urinary Analysis, sums up these conditions and their significance: 



Color. 


Cause of Coloration. 


Nearly colorless. 


Dilution, or diminution 
of normal pigments. 



Dark yellow to 
brown reel. 



Pathological Condition. 



Increase of normal, or occur- 
rence of pathological, 
pigments. 



Nervous conditions : 
hydruria, diabetes insipidus, 
contracted kidney. 



Acute infectious diseases. 



Milky. 



Fat-globules. 



Chyluria. 



Pus-corpuscles. 



Suppurative diseases of the 
urinary tract. 



Orange. 



Eed or reddish. 



Excreted drugs. 



Santonin, chrysopbanic acid, 
senna. 



Uncbanged bsemoglobin. 



Haemorrhages, 
or hsernoglobinuria. 



Pigments in food (logwood, 
madder, bilberries, fuchsin). 



Brown to 

brown black. 



Hseinatin. 



Small hemorrhages. 



Metbsemoglobin. 



Methasmoglobinuria. 



Melanin. 



Melanotic sarcoma. 



Hydrochinon and catechin. 



Carbolic-acid poisoning. 



Greenish yellow, 
greenish brown, ap- 
proaching black. 



Bile-pigments. 



Jaundice. 



Dirty green 
or blue. 



A dark -blue scum on sur- Cholera, typhus ; seen es- 
face, with a blue deposit, due pecially when the urine is 



to an excess of indigo-forming 
substances. Indol. Methylene 
blue. 



Brown yellow to 
red brown, becom- 
ing blood red upon 
adding alkalies. 



Substances which are intro- 
duced into the system with 
senna, rhubarb, and cheli- 
donium. 



putrefying. 



23 



354 THE URINARY BLADDER AND THE URINE 

If the discoloration of the urine be due to blood rather than to 
hemoglobin, a microscopic examination will reveal red blood 
corpuscles, white blood corpuscles, and perhaps fine filaments 
of clots; but the corpuscles will not be found in rouleaux, as in 
ordinary blood outside the body, and they may be crenated and 
distorted in shape, particularly if the urine is alkaline. 

Dark Urine not Due to Blood. — If the urine be red from other 
causes than blood, this may be due to the ingestion of hema- 
toxylon. The history of the ingestion of this substance will clear 
up the diagnosis. If it be due to senna, it will be carmine, due 
to the chrysophan in this drug; but this discoloration only appears 
if the urine is alkaline. Precisely similar changes are due to the 
taking of rhubarb. So in santonin poisoning a blood-red urine is 
sometimes seen, but it usually attains this appearance after being 
at first yellow, then saffron, and then purple red. One of the 
conditions of the urine, due to a poison, which can be readily 
confused with hemoglobinuria or hematuria, is that produced 
by carbolic acid. This color is not due to blood, but to oxidized 
educts of the acid. The same educts produce a similar discolora- 
tion after naphthalin, creosote, and uva ursi have been taken in 
overdose. 

Red urine, due to none of the causes which have been enumer- 
ated, may be due to an excess of urates (except urate of sodium, 
which is usually white). If on the addition of nitric acid the 
urine becomes brown where the fluids join, the coloration is due 
to urates; but if all the fluid is brown, the patient has probably 
been freely taking iodine or compounds of iodine. 

Finally, the urine is often dark reddish brown or porter colored 
in jaundice, owing to the presence in it of biliary coloring matters. 
Under these circumstances it may be clear or opaque, and the 
fluid is apt to be frothy on shaking and to have a decreased surface 
tension, so that powdered sulphur rapidly sinks to the bottom of 
the vessel, when the sulphur is dropped on the urine. These 
biliary colors are at once recognized by the reaction with nitric 
acid in Gmelin's test, for if a little of the urine be placed on a white 
plate and nitric acid be allowed to touch the margin of the wet 
place, a play of colors from green to blue, blue to violet, and 
violet to red occurs. The same test can be used by wetting bibulous 
paper with urine, and the acid, if brought to the edge, will stain 
the paper in the colors named. Green is the only characteristic 
of the biliary reaction, for indican gives with nitric acid the other 
colors/ (For the symptoms of jaundice, see chapter on the Skin.) 

A greenish-colored urine is seen in cases of poisoning by salicylic 
acid, due to the indican and pyrocatechin, and after the use of 
saffron. Not rarely a greenish or blue urine is due to the ingestion 
of methylene blue, either as a medicine, as in the treatment of 
gonorrhea, or in candies colored by this dye. 



* 



THE URINE 355 

Indicanuria is present in intestinal obstruction, intestinal putre- 
faction, cholera, cancer of the liver or stomach, and pernicious 
anemia. It may, however, be present in health as a result of con- 
stipation. When through disease processes indican is formed and 
excreted in the urine, it may by oxidation be transformed into a 
blue color (indigo tin) or into a red hue (indirubin). If the urine 
containing indican be treated with two or three times its volume 
of hydrochloric acid, it will turn a violet hue. 

White or Milky-looking Urine is seen in that condition called 
chyluria, due to the presence of the Filaria sanguinis hominis in the 
blood. This urine on standing forms a creamy layer on its surface, 
and, if it is shaken with ether, some of the fat can be removed, 
rendering the urine clear. This condition can only be confused 
by urine becoming mixed with milk or cream, and the diagnosis 
can always be made if the embryos of the filaria be found in the 
urine. They lie in very delicate sheaths, and show a constant 
vibratory movement. The diagnosis is still further confirmed if 
filaria are found in the blood, where they are present in large 
numbers at night. 

Urine may have a somewhat milky white appearance from an 
excess of phosphates, mixed with more or less mucus, as in 
catarrh of the bladder. A similar appearance may be due to 
the presence of pus. 

Pus. — Should much pus be present in the urine, it is probably 
derived from a pyelitis or a suppurative inflammation of the pelvis 
of the kidney. The symptoms of this state are, briefly, a constant 
or intermittent pyuria, usually an acid reaction of the urine, and 
chills and fever, which may mislead the physician into a diagnosis 
of malarial poisoning. In other cases, if the pyelitis be tuber- 
culous, hectic fever may be present with, sometimes, violent attacks 
of pain resembling renal colic, and not uncommonly anemia 
and loss of strength are notable. There is often pain in the back, 
which is made worse by pressure with the hand, and, rarely, if 
the suppurative process be marked, typhoid symptoms may be 
present. 

If tuberculosis of the kidney is present, tubercle bacilli may be 
found in the urine in addition to pus and blood. The blood at 
times may be present in large quantities. The use of a segregator, 
or ureteral catheter, or the cystoscope may show nearly pure pus 
flowing from one ureter. The discovery of tuberculosis of the 
kidney is of the greatest importance because it is unilateral in 90 
per cent, of the cases according to Bevan and often primary 
so far as the rest of the geni to-urinary tract is concerned. The 
removal of such a kidney, before the general health is greatly 
impaired, may save the patient's life. 

If pyuria is due to a calculus, there may be a history of gravel 



356 THE URINARY BLADDER AND THE URINE 

and renal colic. The purulent urine of pyelitis is to be separated 
from that of cystitis by the fact that in the former the urine is acid, 
in cystitis it is ammoniacal. Additional aids to the diagnosis are 
the pain in the renal region, often unilateral; and the use of the 
cystoscope to exclude vesical disease. The jr-rays may also reveal 
a stone or disease in the renal pelvis. 

(For the chemical and microscopic examination of the urine 
the reader is referred to manuals of clinical chemistry.) 



THE GENERAL SYMPTOMS ASSOCIATED WITH 
URINARY DISORDERS. 

Having considered the pathological changes found in the urine 
and their significance, we now pass on to a consideration of the 
general symptoms which will usually be found associated with 
these variations from the normal functional activity of the urinary 
organs. 

Let us suppose that a patient presents himself complaining 
that he has been seized with pain in the small of the back, and 
perhaps by nausea and chilly sensations, followed by a marked 
decrease in the quantity of urine secreted, which decrease may 
actually amount to suppression of the urine. The urine that is 
passed is high-colored or smoky in hue, sometimes looks like 
porter, and forms a very heavy sediment on standing. If it is 
filtered and tested for albumin, it will be found to contain this 
abnormal ingredient in large amount, and a microscopic examina- 
tion of the sediment will reveal a large number of blood corpuscles, 
epithelial cells, and casts made up of blood cells, epithelium, and 
albumin. Scarcely will these signs have been noted when the 
patient will be seen to be anemic and puffiness of the face about 
the eyes will be evident. This pufiiness may then pass on to a 
general anasarca, but it is to be remembered that the most violent 
acute diffuse nephritis may exist without developing anasarca. If the 
disease be in a child and the illness is due to scarlet fever, anasarca 
is common, as is also uremia. The pulse in patients with this 
form of nephritis is usually hard and tense, and the sharp and clear 
sound of the aortic valves, as heard at the second right costal 
cartilage, will indicate the high arterial tension. The skin is 
generally dry, and, it may be, harsh to the touch. Should the 
symptoms persist for over a month the possibility of the disease 
becoming chronic renders the prognosis doubtful; but, as a rule, 
particularly in young persons, the prognosis of acute diffuse 
nephritis is favorable. In the acute diffuse nephritis of pregnancy 
the prognosis is, of course, grave if the pregnancy continues. 
The history of a case prior to the attack of acute diffuse nephritis 



SYMPTOMS ASSOCIATED WITH URINARY DISORDERS 357 

will usually be that the patient has been exposed to cold or wet, 
has been or is a sufferer from an acute infectious disease, has 
swallowed or inhaled some irritant poison, or has suffered from 
some severe burn of the surface of the body. 

If instead of an acute attack of illness the general symptoms 
just described come on gradually and insidiously, and the tendency 
to anasarca is marked and persistent, we have before us a case of 
chronic parenchymatous nephritis, in which the prognosis is most 
grave. Uremia, vomiting, and coma may occur in this class of 
patients. (See chapter on Vomiting.) Blood cells are also found 
in the sediment of the urine in these cases, but are not so numerous 
as in acute diffuse nephritis. 

A group of symptoms which differ very markedly from those 
just described occurs in cases of chronic contracted kidney (chronic 
interstitial nephritis). The following description of the symptoms 
may be taken as representing a typical case: the patient, who is 
usually past middle life, finds that he or she urinates more fre- 
quently and passes a greater amount of urine than heretofore. 
Often the sleep is disturbed by the necessity of arising to urinate. 
Instead of the urine being heavy and clouded, it is unusually clear 
and limpid; and in place of the high specific gravity of diffuse 
parenchymatous nephritis, we find it unusually low (only i.oio 
to 1.015). Albumin is found only inconstantly and in traces, 
and is generally to be sought for in the urine passed by the patient 
when first arising from bed. The pulse is usually much increased 
in tension, and atheroma of the bloodvessels is more or less marked. 
This high-tension pulse is a valuable diagnostic sign. The heart, 
which in acute diffuse nephritis may be slightly dilated, or in 
chronic parenchymatous nephritis somewhat hypertrophied, is 
in this disease usually markedly hypertrophied, and the second 
sound at the second right costal cartilage is commonly accentuated. 
In addition to these symptoms we find that chronic bronchitis 
is not rare, and that pulmonary edema and attacks of shortness of 
breath, which may be called "asthmatic," are often present, the lat- 
ter being most marked at night. Uremic symptoms are more com- 
monly seen in this class of cases than in any other, and persistent 
vomiting, difficult of control, should always make the physician 
test the urine to discover renal mischief. Unlike parenchymatous 
nephritis, dropsy is a rare complication of chronic contracted 
kidney. Microscopic examination of the urine will reveal only a 
few hyaline and granular casts. The prognosis as to cure is bad, 
but life may be prolonged indefinitely. 

Let us suppose, however, that a patient comes to us with a 
history of exceedingly copious urination, of great thirst, of loss of 
flesh, and has a dry, harsh, skin, we immediately recognize that a 
test of the urine will probably reveal the case to be one of diabetes 



35» THE URINARY BLADDER AND THE URINE 

mellitus. This will be pointed to if a high specific gravity is found 
present in a clear, limpid urine, and confirmed if the tests for the 
sugar produce a reaction. The other prominent symptoms of 
diabetes mellitus are furunculosis, intense itching and erythema 
(see chapter on the Skin), an excessive appetite, and, in some 
severe cases, diabetic coma (see chapter on Coma and Uncon- 
sciousness). 



CHAPTER XIII. 
THE EYE. 

The general diagnostic indications afforded by the eye — Diplopia and disorder 
of the external ocular muscles — Strabismus and squint — Disorder of the 
internal ocular muscles — The pupil — Hemianopsia — The visual fields — 
Color vision — The optic nerve and its lesions — Retinitis — Amblyopia and 
blindness. 

The eye affords more information for diagnostic purposes 
concerning the condition of other organs of the body than any 
single part which can be examined. We gather from it not only 
a clear idea as to its own state, and the state of the nervous centres 
more or less intimately connected with the government of its 
movements and its special functions, but in addition we often 
gain positive information as to the condition of organs more 
remotely situated, as, for example, the kidneys. The very fact 
that so many different tissues are found in this organ renders it 
susceptible to the many diseases affecting similar tissues elsewhere 
in the body. 

The parts of the eye which give us the greatest amount of 
knowledge about changes in other tissues are the optic nerve and 
the retina, its vessels and the ocular muscles. The crystalline 
lens, the conjunctiva, and the cornea often give additional evidence 
indicating the general systemic condition. Cataract should make 
the physician recall diabetes, even when it appears in persons 
advanced in years. The eyelids, if puffy in appearance, may 
indicate renal disease, cardiac lesions, or the overuse of arsenic. 
(See chapter on the Face.) An examination of the inner side of 
the lids may reveal a pallor due to anemia. Slight conjunctival 
hemorrhage may result from violent coughing, and when it is 
recurrent in older persons it should arouse the suspicion of renal 
disease with secondary vascular troubles. 

Prominence of the eyeball, or exophthalmos, is seen as an almost 
constant symptom of exophthalmic goitre. (See Fig. 7.) Associ- 
ated with the bulging eyeball we find more or less enlargement 
of the thyroid gland, an irritable heart, and a very rapid pulse, 
throbbing carotid arteries, marked general nervousness, often 
mental depression, and insomnia. In well-marked or advanced 
cases of exophthalmic goitre we often have a condition in which 
the upper eyelid does not follow the eyeball in its downward 
movement. This is sometimes called "Graefe's symptom." 



360 THE EYE 

Again, the lids may so imperfectly cover the eye that the sclera 
can be seen above and below the cornea, "Stellwag's symptom." 
Or, again, there is insufficiency of convergence, so that a near 
point cannot be seen with both eyes at once (Moebius' sign). 

On examining the exterior of the eyeball, we often notice a 
grayish ring along the junction of the cornea and sclera. It 
possesses, when a complete ring, but little significance, except 
age; but if it is the segment of a ring or in two segments, at the 
upper and lower margins of the cornea, it is a true arcus senilis, 
and is said to indicate in some cases fatty degeneration of the 
tissues of the body. The one is an annulus senilis, the other an 
arcus senilis, and the arcus is the change worthy of note, although 
many clinicians deny that either has much significance. 

An examination of the pupil may reveal that it is immobile from 
an old plastic iritis, due to syphilis or rheumatism, but it is 
not to be forgotten that this condition may arise from iritis 
due to purely local causes. A widely dilated pupil may indicate the 
use of some mydriatic dropped in the eye, or the ingestion of atro- 
pine. Such a pupil is also seen in fright, in some hysterical seizures, 
and in glaucoma and whenever the vision is lost, unless the pupil 
be contracted by disease of the iris. Contracted pupils indicate 
the use of a myotic, the action of opium or the existence of central 
nervous disease, such as ataxia, which causes the Argyll-Robertson 
pupil as well. (See p. 374.) Sometimes corneal inflammation, by 
causing photophobia, may cause excessive myosis. Pin-point pupils 
may also result from the use of opium or its alkaloids, and serve to 
differentiate the condition from true coma, in which the pupils are 
usually dilated. If, however, the coma be due to cerebral inflam- 
mation or meningitis, the pupils may be contracted; or if it be 
due to intracranial pressure, they are usually dilated. (See 
Paralysis of the Intra-ocular Muscles.) 

In addition to these objective symptoms, we have also a very 
important set of signs connected with the ocular muscles, external 
and internal, as manifested by the various forms of strabismus 
or changes in the pupil and in the accommodation of the eye, 
by the ptosis already discussed in the chapter on the Face, and 
in nystagmus and ocular spasm. (See later pages.) Beyond 
this, too, we have two other ocular symptoms, subjective in 
nature, namely, diplopia, or double vision, and partial or complete 
blindness. 

Diplopia depends upon the fact that, in an eye in which the 
muscles are abnormal in their function, the image which falls 
upon the fovea, or visual acuity spot of the retina, in the well 
eye fails to fall upon the same spot in the weak eye. To the well 
eye the object appears to be in the direction in which the eye is 
turned, whereas to the weak eye it appears to be in another direc- 



PARALYSIS OF EXTRA-OCULAR MUSCLES 36 1 

tion. As a result, the mind gets the impression of two objects 
instead of one. The impression made on the well side is the "true 
image," as it is called, and that in the diseased eye is called the 
"false image." Any cause which interferes with the fixation of 
each eye on the same point produces diplopia, and, as the eyes 
are normally directed to the object fixed by the ocular muscles, 
paralysis of any one of these muscles produces diplopia when the 
axis of one eye is deviated from the point of fixation, because 
the eye on one side is not properly moved by reason of the fact 
that one muscle has failed. Diplopia is ordinarily a constant 
sign of ocular muscular paralysis; but if only weakness or insuffi- 
ciency of a muscle is present, diplopia may be a symptom never 
recognized by the patient. The forms of diplopia — that is, the 
position of the false images in respect to the true images — -vary 
with the muscles affected, and will be studied (see below) when 
paralysis of the muscles is tested for and its diagnosis discussed. 
It only remains at this place, therefore, to point out the prob- 
able significance if a patient with diplopia presents himself to a 
physician. 

Thus, a patient with diplopia may be suffering from a lesion in 
the cerebral cortex, such as hemorrhage, sclerosis, or softening; or 
from a lesion in the cranial nerve nuclei, in the pons or corpora 
quadrigemina, or in the fascicular fibers. Again, diplopia may 
arise from lesions at the base of the brain, as meningitis, tuber- 
culous or syphilitic, or from injury to the nerves in the orbit or 
in their peripheral endings. As a result, we find diplopia as a 
symptom of any disease which may affect these parts, and it is 
quite a common symptom in locomotor ataxia, in paretic dementia, 
and in Friedreich's ataxia. Probably it is seen most commonly 
in ataxia, and with it, as the oculomotor nerve in its branch supply- 
ing the levator palpebral is particularly apt to be paralyzed in 
this disease, we may find ptosis. 

Diplopia is also found in cases of ptomain poisoning, and in 
poisoning by belladonna, spigelia, conium, and gelsemium, owing 
to their effects on the oculomotor nerves. 

The differential diagnosis between the various lesions producing 
diplopia is to be made by the other symptoms and the history 
of the case. (See Paralysis of Extra-ocular Muscles.) 

Paralysis of Extra-ocular Muscles. — As something has already 
been said in the chapter on the Face and Head of the diagnostic 
import of paralysis of the ocular muscles in connection with the 
subject of ptosis, a further consideration of the abnormal changes 
in their functions will be discussed first in the present chapter.1 

1 In the preparation of this chapter free use has been made of the excellent 
article of my friend Dr. de Schweinitz, on "Diseases of the Cranial Nerves," in 
Dercum's "Nervous Diseases." 



362 THE EYE 

Before doing so, however, it is necessary to describe the methods 
resorted to for the purpose of demonstrating or determining 
departures from the normal in these muscles. In the first place, 
it must be clearly understood that the function of the extrinsic 
muscles of the eyeball is to direct the ball toward the object at 
which the patient desires to look, and also evenly balance one 
another to keep the eye steady in its axis. Thus the external 
and internal rectus muscles maintain the horizontal equilibrium 
of the eyeball. If the internal rectus is completely paralyzed in 
one eye, we have developed a unilateral external squint, the eye 
looking toward the outer side of the orbit; and if the external 
rectus fails, the eyeball is turned toward the nose. If these muscles 
are affected in both eyes, we have a divergent squint in the first 
case, and a convergent squint in the second. Not only do the 
muscles of each eyeball govern the eye movements of that side, 
but by the nervous centres governing the eye muscles the two 
sets of eye muscles are coordinated, so that they move as one 
organ in health. 

Just here it is well for the reader to make a clear distinction 
between concomitant and paralytic squint, for they are two very 
different things in origin, symptoms, course, and prognosis. A 
concomitant squint is a wrong relation in the visual axes, so that 
they do not intersect in the point looked at; but there is no marked 
limitation of the movements of either eye in any direction. Be 
the direction of the eyes what it may, the squint remains prac- 
tically unchanged. Further, if the fixing eye is covered, the 
other eye promptly fixes, and the covered eye deviates without 
the patient altering the position of the eye (Jackson). On the 
other hand, paralytic squint is the deviation which takes place 
when the attempt is made to turn the eyes in certain directions 
by means of the muscles which are paralyzed in whole or in part. 
When the attempt is made, the eye with the sound muscles turns 
as it should, while the eye with a paralyzed muscle hangs back, 
beginning to deviate as the eyes are turned, so that this muscle 
is required to perform its function, and deviates more as greater 
effort is required. The degree of squint and of separation of the 
double images it causes varies with the direction in which the 
eyes are turned, there being none at all in certain directions. 

We examine the functional activity of the ocular muscles by 
the following measures: 

The patient is told to look at the tip of a pencil or the tip of the 
finger of the physician, held about three feet from his face. This 
object is then gradually brought nearer and nearer to him, and 
the eyes of the patient necessarily converge more and more as it 
approaches his nose. Normally, the eyes will be coordinate^ 
converged when the object is only three and a half inches from 



PARALYSIS OF EXTRA-OCULAR MUSCLES 



363 



them; but if any weakness or insufficiency of one internus is 
present, the eye on that side will deviate or fail to converge before 
this point is reached. 

Again, a fine point, like a pin-point, is held at about eight or 
ten inches from the eyes and below the horizontal, and one eye 
is covered by a card or hand. If the eye which is separated from 
the object by the card deviates inward, it indicates insufficiency 
of the external rectus. If, on the other hand, it deviates outward, 
it shows insufficiency of the internal rectus. On sudden removal 
of the card the eye at once springs back into place for the purpose 
of fixing upon the object, and "in general terms each millimeter of 
movement deviating from the fixation point corresponds to what is 
called 2 degrees of insufficiency as measured by prisms." (Randall.) 
If the internus is insufficient, and the covered eye moves in to fix 
in several distinct impulses, each impulse should be multiplied 
into the foregoing result. 

A very useful, and the simplest, apparatus for testing the func- 
tional balance of the ocular muscles is the rod test of Maddox. 



B 



■~-~\ =;- 



m 

11 ■ 

W m m 

■LJB 


1 




n 


fl 1 

in I 

1 ■ E 

ill 

I ■ Kg 




1 


i ; 




BH 



■ 


i 


; 


1 



Fig. 131. — Maddox's rod test for horizontal deviation. The rod is before the 
right eye. A. The line passes through the flame — orthophoria. B. The line 
passes to the right of the flame — latent convergence, or esophoria. C. The line 
passes to the left of the flame — latent divergence, or exophoria. (de Scrrweinitz.) 



A cell, in which is mounted a transparent glass rod, is placed 
in a trial frame, which is then placed in front of the eyes. If the 
horizontal deviation is to be determined the physician should "seat" 
the patient at six meters from a small flame, and place the rod 
horizontally before one eye, a colored glass before the other. If 
the line passes (vertically) through the flame there is orthophoria 



364 



THE EYE 



(equipoise), so far as the horizontal movements of the eye are 
concerned. Should the line lie to either side of the flame, as 
in most people it will, there is either latent convergence or latent 
divergence: the former if the line is the same side as the rod 
(homonymous diplopia), the latter if to the other side (crossed 
diplopia) (Fig. 131). 

When the vertical deviation is to be estimated, the rod is placed 
vertically in the frame. If the patient states that the horizontal 
line of light passes directly through the flame, the vertical balance 
of the eyes is normal; if, on the other hand, the line is above the 
flame, there is a tendency to upward deviation of the naked eye; 
but if the line is below the flame, there is upward deviation of 
the eye covered by the rod (Fig. 132). Testing of this kind 
refers to the insufficiencies and not to the palsies of the ocular 
muscles. 



Hi 





£ 


n 


w~ 




Fig. 132. — Maddox's red test for vertical deviaticn. The rod is before the 
right eye. A. The line passes through the flame — orthophoria. B. The line 
passes below the flame. The upper image belongs to the left eye — right hyper- 
phoria. C. The line passes above the flame. The upper image belongs to the 
right eye — left hyperphoria, (de Schweinitz.) 

The importance of being able to demonstrate these minor 
failures in the ocular muscles by these means lies in the fact that 
in this manner headaches due to muscle eye-strain may be remedied 
by removing their cause by properly fitted glasses, or by gymnastic 
exercises with prisms, or, in some cases, by tenotomy. 

Where there are marked palsies of the ocular muscles, there is 
usually some poison exercising its effects upon their nervous 
centres or the nerves themselves, or there is some central nervous 
lesion affecting the centres governing these muscles in the cortex, 
or there is a lesion in the nuclei or fasciculi, or, again, there may 
be lesions in the basal ganglia, or in the course of the fibers of the 



PARALYSIS OF EXTRA-OCULAR MUSCLES 365 

nerve between the nucleus and the eye, or in the orbit or nerve 
endings. 

The signs of paralysis of the ocular muscles consist in the follow- 
ing symptoms: Diplopia, which is due to the failure of the images 
to fall on the corresponding points in each retina. This diplopia 
becomes more and more marked as the object moves toward the 
side on which the paralzyed muscle lies. Strabismus, which may 
or may not be constant, usually develops when the patient 
endeavors to turn his eyes in the direction of the paralyzed muscle. 
Vertigo, which is due to the diplopia, or, if the well eye is closed, 
to an erroneous localization of the objects in the field of vision. 
Altered carriage of the head, due to the fact that the patient 
tries to turn his head in the direction in which he is least 
troubled by double images — that is, he obtains the natural fix- 
ation point of the weak eye, and then adjusts the well eye 
accordingly. 

If the paralysis of the ocular muscle be complete, the squint 
and the loss of movement of the muscle which is paralyzed will 
usually enable the physician to find out the paralyzed muscle; 
but if there be only a partial paralysis of an ocular muscle, then 
squint is not necessarily present, and the diagnosis of the part 
affected must be made by a study of the double images. This is 
made by placing before the patient, at a distance of from three 
to five yards, a candle on the same level as his eyes. One eye is 
covered by a piece of red glass, so that the patient can readily 
distinguish between the images. The lighted candle is then moved 
from the middle line of the patient to the right and left, and the 
relative positions of the red and white images are noted. Then 
the candle is moved up and down, and the results recorded. These 
operations having been recorded, it is to be remembered that 
diplopia is most marked and sometimes only appears when the 
patient turns his eyes in that direction which calls into play the 
affected muscles, no diplopia being present if other muscles are 
used. Again, the image which belongs to the affected eye is pro- 
jected in the direction toward which the paralyzed muscle normally 
turns the eye, and, finally, the distance of the double image 
increases when the eyes are turned in the direction of the action 
of the paralyzed muscle, or, in other words, that image is false 
and belongs to the affected eye which in the region of diplopia 
moves faster than the moving test object — that is, the candle 
flame. 

If there is divergent squint with failure of movement in all 
directions, except outward and slightly downward, and there are 
ptosis, moderate mydriasis, and paralysis of accommodation, 
there are oculomotor paralysis and crossed diplopia. 

It is exceedingly difficult always to localize exactly the affected 



366 THE EYE 

muscle, especially when more than one is paretic, the paresis being 
of different degrees. 

Paralysis of the ocular muscles may be due to a lesion in one of 
several places. Thus it may arise from hemorrhage, sclerosis, and 
softening of the cerebral cortex, in which case the other symptoms 
of lesions in those parts will be present as in apoplexy, disseminated 
sclerosis, or meningeal disease. Or it may depend upon lesions in 
the fasciculi between the cortex and the nuclear origin of the 
nerves, as in the crus. This is rare. Or, again, it may be due to 
lesions in the nuclei. If this be the case, we have developed 
ophthalmoplegia, 1 or paralysis of all the ocular muscles supplied 
by the third, fourth, and sixth nerves. This nuclear paralysis 
is divisible into two classes, the acute and chronic. Sometimes 
it is called acute and chronic nuclear palsy. The acute form is 
sudden in its onset, all the ocular muscles losing power. With 
the onset of the attack there may be fever, vomiting, and even 
convulsions. Such an attack results from minute hemorrhages 
among the nuclei, or from an acute hemorrhagic polioencephalitis 
in the fourth ventricle, arising from syphilis, tuberculosis, ptomain 
poisoning, alcoholic, and sulphuric acid poisoning. Such cases 
are usually rapidly fatal. A less fatal form follows injuries, and 
the effects of nicotine, lead, carbonic oxide, or such diseases as 
diabetes, syphilis, and epidemic influenza. Sometimes acute 
ophthalmoplegia comes on with acute poliomyelitis or acute 
bulbar paralysis. 

Chronic nuclear paralysis is gradual in its onset, muscle after 
muscle failing, and even ptosis coming on. Sometimes, after a 
certain degree of paralysis is reached, the disease comes to a 
standstill. The trouble may be unilateral or bilateral, and is 
often unsymmetrical, and it occurs after acute ophthalmoplegia, 
as a congenital defect producing bilateral ptosis (see chapter on 
the Face), as an acquired disease in childhood and adult life, 
and in conjunction with locomotor ataxia, paretic dementia, dis- 
seminated sclerosis, progressive muscular atrophy, chronic bulbar 
paralysis, and in connection with paralysis of the frontalis and 
orbicularis palpebrarum, which are innervated by the facial nerve. 
The cause may be tuberculosis or syphilis, but in some cases no 
cause can be found. 

If the cause of the paralysis of one or two muscles be basilar 
lesions, these may arise from hemorrhage, pachymeningitis, menin- 
gitis, both simple and tuberculous, chiefly the latter; purulent 
meningitis, abscess as the result of middle-ear disease, and anemia. 
It may also arise as the result of obliterating arteritis, particularly 

1 Ophthalmoplegia is here applied in its strict sense. The word is often used 
to signify loss of power in individual eye muscles; and while its use in both ways 
is correct, it is better to confine its usage to nuclear and complete lesions. 



PARALYSIS OF EXTRA-OCULAR MUSCLES 367 

in syphilitics, and from tumors. The frequency with which palsy 
of the ocular muscles depends on syphilis is noteworthy. Alexander 
asserts that 75 per cent, of all cases of unilateral paralysis of the 
third nerve are due to syphilis, and Uhthoff states that only about 
15 per cent, of the cases of cerebral syphilis escape some ocular 
palsy. In children, sudden convergent strabismus and diplopia 
are often among the earliest symptoms of tuberculous meningitis 
at the base of the brain due to pressure on the roots of the sixth 
nerve. 

If the cause be in the nerve trunks themselves, the lesion will 
probably be cellulitis, tenonitis, hemorrhages in the orbit, or frac- 
tures of the orbit; or, again, there may be disease of the frontal 
sinus. If the lesion is distinctly peripheral, it may be due to 
rheumatism (when the external rectus is commonly affected), 
neurasthenia, or it may arise from lithemia and gout. Further, 
such lesions may be due to influenza, diabetes, diphtheria, lead, 
and alcohol, or any one of the drugs which paralyze the ocular 
nerves. 




Fig. 133. — Paralysis of left abducens in a case of hemiplegia of syphilitic 
origin. (Dercum.) 

So much for general statements as to the common and possible 
sites of the lesions producing paralysis of the ocular muscles. We 
can now go farther than this, and locate the lesion more accurately 
from the knowledge we have gained as to particular muscles affected 
and the other symptoms presented by the case. 

Let us suppose that a patient suffering from paralytic internal 
squint or a diplopia which indicates paralysis of the external rectus, 
presents himself to the physician, what diagnostic significance 
has this symptom? 1 

In the first place, it is to be remembered that the external rectus 

1 This refers to paralytic and not to concomitant squint. 



368 THE EYE 

receives its nerve supply from the abducens, or sixth nerve (Fig. 
133), which arises from the pyramidal body close to the pons. 
(See Plate II and Fig. 6.) Its deep origin is a nucleus under the 
floor of the fourth ventricle. The nerve pierces the dura mater 
on the basilar surface of the sphenoid bone (see Plate VI), 
passes through the clinoid process, enters the cavernous sinus, and, 
finally, enters the orbit through the sphenodial fissure between 
the heads of the external rectus. If this form of squint is associated 
with hemiplegia of the opposite side of the body, the lesion is in 
the pons on the same side as the affected eye and the opposite 
from the hemiplegia, because the eye fibres have crossed higher 
up, but the motor tracts for the limbs cross Jower down. 

On the other hand, if there is monoplegia and abducens palsy 
(internal squint) on the same side of the body, the lesion is in the 
point of origin of the abducens and arm centre in the cortex, or, 
in other words, the lesion has taken place above the point where 
the tracts cross. Such a paralysis is, therefore, cortical. 

If, again, there is complete unilateral paralysis of the abducens 
(internal squint) with loss of the associated action of the internus, 
the lesion is in the nuclei under the floor of the fourth ventricle, 
because the nuclei of the third and sixth cranial nerves are closely 
connected, so that a lesion involving the sixth nucleus weakens the 
nucleus of the third nerve. Complete paralysis of the externus 
may, therefore, be due to a nuclear lesion; for if the lesion were 
above the nucleus, this nucleus might obtain collateral impulses, 
and, therefore, the paralysis would be only partial. It may also 
be due to a peripheral lesion and sometimes an inflammatory 
process pressing upon the basilar surface of the sphenoid, and 
thereby involving the nerve, may cause a similar effect. Loss of 
power of the external rectus may also arise from neurasthenia, 
gout, and rheumatism, and in tuberculous or syphilitic meningitis 
at the base, as already stated. It also comes on in some cases of 
diabetes, la grippe, and in chronic poisoning by lead and alcohol, 
or the acute poisoning of gelsemium, ptomain poisoning, conium, 
and spigelia poisoning. 

Again, let us suppose that the internal rectus is paralyzed, causing 
external squint. We remember that it is supplied by the oculo- 
motor nerve, which springs from the inner side of the crus close 
to the upper border of the pons (see Fig. 6 and Plates I and II), 
very near the roots of the fourth and sixth nerves. It arises from 
several roots. The nerve itself pierces the dura mater below the 
posterior clinoid process, passes along the outer wall of the cavern- 
ous sinus, and after dividing into two branches enters the orbit 
through the sphenoidal fissure. (See Plates I and VI.) The upper 
branch supplies the superior rectus and the levator palpebrae, 
and the lower one, after dividing into three branches, supplies the 



PARALYSIS OF EXTRA-OCULAR MUSCLES 369 

internal rectus, the inferior rectus, and the inferior oblique muscles. 
(See Plate V.) The oculomotor nerve receives filaments from the 
cavernous plexus of the sympathetic and from the first division 
of the fifth nerve. In addition to divergent squint there are, as 
already pointed out in the last few pages, in oculomotor par- 
laysis, as additional symptoms, ptosis, mydriasis, and paralysis of 
accommodation. 

The lesion producing unilateral ptosis may be found in the cere- 
bral cortex on the opposite side from the affected eye in the angular 
gyrus just below the interparietal fissure. Again, tuberculous or 
other degenerative disease of the corpora quadrigemina may cause 
double ptosis. 

If the patient has ptosis with preservation of the function of the 
intra-ocular muscles (that is, partial oculomotor paralysis), with 
hemiplegia of the opposite side of the body, the lesion, according 
to Mauthner, probably affects the fascicular fibres — that is, those 
between the cortex and the nuclei. There may be associated with 
this form of oculomotor paralysis loss of power in the hypoglossal 
and facial nerves. On the other hand, if the oculomotor paralysis 
is complete, the lesion is almost certainly at the base of the brain, 
and this diagnosis becomes practically certain if there is associated 
with it paralysis of other cranial nerves. Paralysis of the oculo- 
motor nerve on one side with hemiplegia on the opposite side of 
the body is not positively a crus or fascicular lesion unless the 
paralysis occurs simultaneously (Hughlings Jackson). 

If, however, there be double oculomotor paralysis, the lesion is 
bilateral and probably due to a lesion at the base, as meningitis 
or arteritis (see Plate I), or to an inflammatory exudate involving 
both nuclei; or, again, to diphtheritic poison, or the lesions of tabes 
dorsalis. 

If that very rare form of ocular muscle paralysis, namely, 
isolated palsy of the fourth, or trochlear, nerve, is present, we will 
probably find that the paralysis is due to a lesion at the base of 
the brain, due to meningitis, or the pressure of a growth. 

Supposing, however, that a patient presents himself with swelling 
of the eyelids, exophthalmos, a contracted followed by a dilated 
pupil, anesthesia of the skin of the upper eyelid and of the temple, 
or the area supplied by the first division (ophthalmic) of the fifth 
nerve, and ophthalmoplegia — that is, paralysis of the extrinsic 
ocular muscles on one side — Where will be the lesion productive of 
this train of interesting symptoms? It will be seen at once that 
such a condition is the result of paralysis of the oculomotor (third), 
pathetic (fourth), and abducens (sixth) nerves, and that, as in all 
probability, only one lesion has produced these symptoms, it must 
exist at some point where all these nerve fibres are so closely 
approximated that they are readily involved together. It will be 
24 



37° 



THE EYE 



recalled that the course of these nerves is as follows: The oculo- 
motor nerve, having arisen from the nucleus in the corpora quad- 




Sphincter iridis. 
Musculus ciliaris. 
Convergence centre. 
Rectus superior. 
Rectus internus. 
Levator palpebrae superiors. 
Obliquus inferior. 
Rectus inferior. 

Obliquus superior. 



Rectus externus. 



Fig. 134. — Scheme of the nuclei of the nerves of ocular movement and of their 
central and peripheral tracts: R, right eye; L, left eye; C, chiasm; On, optic 
nerve; Ot, optic tract; Q, pregeminum (anterior quadrigeminal body); P, cortical 
centre for the movement of elevation of the upper eyelid; M, cortical centre for 
ocular movements; Tn, course of all ocular nerves in the cavernous sinus. The 
names of the different nuclei are printed on the diagram, and the nerve tracts 
going from these nuclei can be readily traced to where they converge in their 
course in the cavernous sinus and where they diverge to pass the various 
muscles of the eye. The dotted lines represent associating and commissural 
tracts, showing how the fibres of the third, fourth, and sixth nerves come together 
in one bundle in the cavernous sinus. (From Mills' Nervous Diseases.) 



rigemina, pierces the dura mater below the posterior clinoid process, 
passes along the outer wall of the cavernous sinus, and there divides 



PARALYSIS OF EXTRA-OCULAR MUSCLES 37 1 

into two branches. The pathetic nerve passes near the clinoid 
process along the outer wall of the cavernous sinus, and with the 
oculomotor nerve enters the orbit through the sphenoidal fissure. 
The sixth nerve pierces the dura mater on the basilar surface of 
the sphenoidal bone, passed through the clinoid process, and enters 
the cavernous sinus, finally reaching the orbit through the sphe- 
noidal fissure. It is thus seen that a lesion at the sphenoid fissure 
and pressure in the cavernous sinus would cause all the symptoms 
described above. (See Fig. 128 and Plates I and VI.) This 
occurs in cases of thrombosis of the cavernous sinus. Where there 
is an arteriovenous aneurysm of this sinus there will be pulsating 
exophthalmos. Injury or inflammation, if in this area, may also 
produce a series of symptoms. 

The significance of conjugate lateral paralysis producing a devia- 
tion of both eyes to the right or left, as the case may be, is that some 
lesion exists in the cerebral cortex, the corona radiata, or the internal 
capsule, or in the pons before the fibres have crossed. The lesion, 
if in the cortex, however, does not have to be localized in one spot, 
for any source of irritation in the cortex may apparently cause 
conjugate deviation. If the lesion is the result of an apoplexy, the 
eyes are turned toward the side opposite to the paralysis (Prevost's 
symptom) — that is, the " patient looks at his lesion." The reason 
that a unilateral lesion can cause a bilateral deviation is that the 
lateral movements of the eye are governed by an impulse which 
passes down from the cortex to the sixth nerve nucleus, and thence 
across the posterior longitudinal fasciculus to the opposite side, 
where it passes to the nucleus of the third nerve. As conjugate 
lateral deviation is caused by contraction of the internal rectus 
on one side (third nerve) and the external rectus on the other (sixth 
nerve) the mechanism of the deviation is clear. Thus, if the 
lesion be a distinctive one on the left side of the brain, causing 
right hemiplegia, the eyes will be turned to the left by the action 
of the unaffected left external rectus and the right internal rectus; 
while if the lesion be on the right side of the brain, the reverse 
will occur. If, however, the lesion be irritative (as a tumor), this 
deviation is reversed, because in this case the centres are irritated 
and cause spasm of the muscles receiving their nerve supply from 
the affected side of the cerebrum. In other words, the eyes are 
turned toward the side of the body which is convulsed. 

In the first instance the eyes are turned away from the affected 
side because the muscles of the eyes on that side are also paralyzed, 
and the eyes are, therefore, turned by the muscles which remain 
intact. In the second instance the eyes are turned toward the 
convulsed side because the internal and external rectus are spas- 
modically contracted and so overcome the healthy muscles. 

We find, however, that if the lesion be in the pons rather than 



372 



THE EYE 



in the cortex, these conditions are reversed, for now a destructive 
lesion causes the eyes to be turned to the paralyzed side, and an 
irritative lesion directs them away from the paralyzed side. 

This is best explained by the following diagram and description 
from Swanzy's well-known book (Fig. 135). 




Fig. 135. — 1. Left ext. rectus. 2. Left int. rectus. 3. Right int. rectus. 
4. Right ext. rectus. 5.^ Nucleus left third nerve. 6. Nucleus right third nerve. 
7 and 8. Post, longitudinal bands from sixth nerve to opposite third nerve. 9. 
Nucleus left sixth nerve. 10. Nucleus right sixth nerve. 11 and 12. Left and 
right cortical centres. An impulse starting from 12 would travel down to 9 
and produce an associated movement of the eyes to the left. 



A destructive lesion at twelve, the right cortical centre, involving 
also motor centres of the body, would cause left hemiplegia; and 
since the external rectus of the left eye and internal rectus of the 
right eye would be paralyzed, the antagonists would turn the eyes 
to the right — i. e., away from the paralyzed side. A destructive 
lesion of the right side of the pons, also producing left hemiplegia, 
if it involves the sixth nuclues, will produce paralysis of the external 
rectus of the right eye and of the internal rectus of the left eye, and 
then the antagonists would turn the eyes to the left — i. e., toward 
the paralyzed side. It is easy to see how irritative lesions would 
produce exactly the opposite effects. 

Squint which is due to hysteria is always caused by spasmodic 
contraction of the eye muscle and is never due to paralysis, as it 
often is in organic disease. Very often there is a spasm of the eyelid 
or eyebrow associated with it. The administration of a relaxant, 
such as chloroform, will at once overcome such a squint. 

Nystagmus, or the rapid oscillation of the eyes from side to side 
or in a vertical or rotary movement, is usually bilateral. 1 When 
not congenital it is a frequent symptom of disseminated sclerosis, 

1 The physician should remember that some occupations, such as mining, pro- 
duce in some persons nystagmus without the presence of the disease about to be 

named. 



TESTING THE PUPIL 373 

Friedreich's ataxia, advanced locomotor ataxia and labyrinthine 
disease; and while it does not localize the lesion, it indicates very 
positively that one is present and that the case is not one of hysteria 
or funtional disease. Nystagmus occurring in children is very 
often associated with imperfect vision of great degree or with 
blindness as a result of opacity of the cornea, congenital cataract, 
or atrophy of the nerve. In other instances, however, it arises 
from growths in the cerebellum or pons, and it is sometimes seen 
in hydrocephalus and very rarely in acute meningitis and in 
epilepsy. Very rarely lateral nystagmus is seen in children who 
seem otherwise normal, and it then possesses no particular diag- 
nostic importance. 

Paralysis or Disorder of the Intra-ocular Muscles. — Having 
discussed the diagnostic indications of changes in the functions 
of the extra-ocular muscles, we next proceed to a consideration of 
these facts in connection with the intra-ocular muscles. These 
consist, it will be remembered, in the muscular fibres of the iris, 
circular, and radiating, and the ciliary muscle. The nerve supply 
of the iris consists in fibres from the oculomotor or third nerve, the 
upper or ophthalmic division of the fifth, and the sympathetic. 
It will be remembered that in the posterior part of the orbit there 
is situated a ganglion called the ciliary or ophthalmic ganglion. 
By its short or motor root this ganglion is connected with the 
third nerve, by its sympathetic root with the cavernous sympathetic 
plexus and the cervical sympathetic plexus, while by its long or 
sensory root it is connected with the nasal branch of the ophthalmic 
or upper branch of the fifth nerve. From this ganglion extend 
forward two sets of nerves, one short (the short ciliary nerve), 
which supplies the iris and the ciliary muscle, and one set long 
(long ciliary nerves), which also go to the iris. The filaments 
which go to the ganglion by means of its short or motor root 
(from the oculomotor nerve) pass forward to the circular fibres 
of the iris, while those which have arisen in the sympathetic 
plexus pass forward to the radiating fibres. These last fibres are 
in part derived from the cervical sympathetic ganglion, run through 
the carotid plexus, and are controlled to some extent by the cilio- 
spinal centre of Bunge in the spinal cord at about the seventh 
cervical or first dorsal vertebra. 

The ciliary muscle is supplied by the fibres of the short ciliary 
nerves, which have arisen in the floor of the third ventricle and 
which is connected with the nucleus of the third nerve. 

Testing the Pupil. — The normal pupil is about 4 mm. in diam- 
eter, but this varies according to the degree of light to which the 
patient is exposed. It ought always to be measured by a millimeter 
measure, which gives its approximate diameter. 

The pupil to be tested must be free from any abnormal conditions 



374 THE EYE 

produced by new or old inflammation of the iris, and the light used 
should not be excessively bright, but about that usual to the eye. 

The patient is to be placed facing the light and told to look at 
some distant object. The hands of the physician are then placed 
one over each eye, the patient being told to keep his eyes open. 
One hand is now quickly removed from one eye and the pupil 
observed. This observation must be acute or the pupillary contrac- 
tion will occur before it is seen. This reflex is due to the fact that 
we have an irritation of the optic nerve by light, and this sends a 
reflex wave to the centres governing the pupil and causes it to 
contract. Not only does the uncovered pupil react in this manner, 
but the covered one does the same thing. The first is called a 
direct reflex, the second is called the indirect or consensual reflex. 
The exact pathway of this reflex is unknown. 

Not only does the pupil change its size by reason of the ordinary 
light reflex, but it also contracts or dilates in association with the 
other muscles governing accommodation and convergence, namely, 
the ciliary muscle and internal recti. This is the associated reaction 
of the pupils, and is tested by causing the patient to direct his 
eyes to a near object — for example, the point of a pencil. If the 
sign is intact, contraction of the pupil will occur. 

The pupil-dilating centre is in the medulla and is very sensitive 
to reflex irritation. 

Abnormal Pupillary Movement. — Supposing that the pupillary 
movement is abnormal, we should recollect before studying the 
case further what the causes of its perversion may be. Thus, its 
size is altered by drugs, by local disease of the iris, by spinal dis- 
ease of the sympathetic, by localized cerebral lesions, by abeyance 
of the cerebral functions, and by irritation of the brain. Let us 
suppose, however, that on testing the ocular reflexes in the manner 
already described we find that the pupil of one eye when uncovered 
does not contract, and immediately does so as soon as the other 
eye is uncovered, What is the indication? It indicates that there 
is disease of the optic nerve of that eye which does not convey the 
impulse of light from the retina; whereas, if it contracts when the 
other eye is uncovered, it shows that the rest of the mechanism 
involved in the reflex is intact. Accommodative reaction of the 
pupil is intact also. 

If the irides fail to react to light, but do to accommodation and 
convergence, we have the " Argyll-Robertson pupil," so called, 
which indicates that a lesion exists in the fibres back of those 
concerned with the ordinary light reflex. 

This condition is seen in locomotor ataxia, general paralysis 
of the insane, sometimes in cerebral syphilis, and as the result of 
poisoning by the bisulphide of carbon. Grube has reported three 
cases in which the Argyll-Robertson pupil developed in the course 



ABNORMAL PUPILLARY MOVEMENT 375 

of diabetes mellitus. Marinesco has reported an instance of Argyll- 
Robertson pupil in a patient suffering from amyotrophic lateral 
sclerosis. It is worthy of note, however, that late in all these 
affections the reaction to accommodation may also be lost. Rarely 
the reverse of the Argyll-Robertson pupil occurs as the result of 
a lesion in the second and third parts of the oculomotor nucleus. 
If the eyes fail to react to light and to accommodation, there is 
probably blindness due to optic nerve disease. 

If on throwing light into the right eye there is no reaction of 
the pupil of that eye, and on throwing it into the left eye there 
is still no reaction in the pupil of the right eye, there must be a 
lesion of the nucleus of the right oculomotor nerve or palsy of the 
conducting fibres of each optic nerve. 

Sachs asserts that immobility of the pupil is very characteristic 
of syphilitic cerebrospinal disease, and if the diagnosis lies between 
multiple sclerosis on the one hand, and cerebrospinal syphilis on 
the other, the discovery of immobility of one or both pupils should 
decide in favor of its being a syphilitic case. He also asserts that 
persistent pupillary immobility in a case of hemiplegia indicates a 
syphilitic endarteritis. It is important in this connection to re- 
member that the pupillary changes due to syphilis often suddenly 
improve, while those due to sclerosis are absolutely permanent. 

Contraction of the pupil occurs in a large number of conditions 
and yet possesses considerable diagnostic significance. Thus it is 
generally found in the early stages of all acute inflammatory 
processes in the brain or its membranes. In cerebral hemorrhage 
it is usually contracted at first, thus serving to separate acute 
paralysis due to hemorrhage from that due to embolism, for in the 
latter Berthold states that the pupil is unaltered. In the early 
stages of intracranial tumors which irritate the third nerve nucleus 
it is also contracted. Finally, we find myosis as a result of chronic 
tobacco poisoning, from irritation of the pupil-contracting centre 
by nicotine, at the beginning of an attack of hysteria or epilepsy, 
and in watchmakers and jewellers. Such forms of myosis are 
called " irritative myosis." Myosis is also seen in disease of the 
apex of the lung. (See next page.) 

Paralytic myosis is met with in lesions above the dorsal vertebra 
of a chronic type, as a rule. Its most interesting form is that seen 
in locomotor ataxia, when the disease has involved the ciliospinal 
centre. 

Of course, pupillary contraction may result from the action of a 
myotic .drug, as eserine or pilocarpine. 

Dilatation of the pupil may also be due to irritation or paralysis. 
Thus, irritation of the pupil-dilating centre may cause mydriasis, 
and this is met with in congestion of the cervical spinal cord and in 
spinal meningitis, as the result of tumors in the cervical cord, in 



376 THE EYE 

spinal irritation, in the anemia of convalescence, as an early sign of 
tabes dorsalis, and in acute mania. Certain cases of acute croupous 
pneumonia present dilatation of both pupils, the dilatation being 
most marked on the affected side, probably by irritation of the 
sympathetic fibres by pressure of the consolidated lung. Sometimes 
in progressive paralysis of the insane there may be irritative 
mydriasis in one eye and myosis in the other. Von Graefe asserts 
that alternating unilateral mydriasis is an early sign of mental 
derangement. 

The states in which we find paralytic mydriasis are in the later 
stages of progressive paralysis, in lesions at the base affecting "the 
oculomotor centre, late in thrombosos of the cavernous sinus, in 
orbital disease which causes pressure on the ciliary nerves, in 
glaucoma, and in intracranial growths of considerable size. Not 
only may paralytic mydriasis be due to an oculomotor lesion, but 
as the result of some blocking of the pathway from the retina to 
the centre. 1 

Under the name of " hemiopic pupillary inaction :■," or "Wernicke's 
pupil," we sometimes, though rarely, meet with a condition asso- 
ciated with hemianopsia, or blindness in one-half of the eye, which 
is demonstrated in the following manner: The patient is seated in a 
dark room and one eye is covered. The other eye is now illuminated 
by just sufficient light from a flat mirrir to enable the physician to 
see the eye. By means of the concave mirror of an ophthalmoscope 
the physician now directs into the uncovered eye a bright beam of 
light, taking care that it falls upon one side of the retina, or, in 
other words, enters the eye obliquely and strikes on the side of the 
retina which is blind. If when the light falls on the blind side of 
the retina there is no pupillary reaction, it is considered that the 
lesion exists in the arc between the optic chiasm and the corpora 
quadrigemina; but if there is a pupillary reaction, the lesion must 
be farther back in the visual centres, back of the reflex arc. When 
the lesion is found back of the reflex arc it may indicate a lesion 
of the optic tract, the posterior segment of the thalamus, the 
posterior part of the chiasm, or rarely it may be caused by a lesion 
of the optic nerve if the hemianopsia be monocular, which is rarely 
the case. 

Finally, a rhyth m ical contraction and dilatation of the pupil, 
called 'hip pus" is seen in health for a moment on sudden exposure 
to light; but when constant is a sign of disseminated sclerosis, 
hysteria, epilepsy, or the early stages of acute meningitis. 

The presence of a recurrent, unequal dilatation of the pupils of 
a transitory character is said by Rampoldi to be an early and almost 

1 For a useful summary of these facts and for references, see "Diseases of the 
Eye," by Swanzy, sixth edition. 



CHANGES IN THE ACUITY OF VISION 377 

constant sign of pulmonary tuberculosis. He believes that this is 
due to a reflex irritation of the nerves governing the pupil through 
the sympathetic system. Probably in these cases enlarged glands 
in the chest are the cause of pupillary phenomenon. Destree 
claims that 97 per cent, of his cases of phthisis present this pupil- 
lary symptom. On the other hand, Souques asserts that myosis 
is commonly present in tuberculous apical disease owing to the 
dilator fibres from the ciliospinal centre which pass through the 
first dorsal nerve to the cervical sympathetic being pressed upon 
by the apex of the pleura. Evidently it is an irritative reflex, 
and results in mydriasis or myosis, according to the degree of 
pressure. 

Knies points out that pupillary contraction and dilatation take 
place in association with Cheyne-Stokes breathing. Dilatation 
usually exists with the inspiratory movements, and myosis occurs 
during the interval of apnea. 

Changes in the Acuity of Vision. — Having discussed the diag- 
nostic value of alterations from the normal in the function of the 
extra- and intra-ocular muscles of the eye, we can proceed to a 
consideration of the value of changes in the acuity of vision. The 
questions of the acuity of vision in relation to errors in the 
refractive media of the eye will not, of course, be included in this 
book. 

Failure of vision in part or in toto depends upon a lesion which 
destroys the peripheral ocular sense organ (the eye), the optic 
nerves, the optic tracts, or the receptive and perceptive centres 
of sight. It also is dependent upon bilateral lesions in the crystal- 
line lens, as in cataract, or in the cornea, as in severe keratitis. 

Before we discuss these various causes of blindness it is necessary 
that we recall the nervous anatomy of the organs of sight. These 
nerve fibres starting with the rods and cones of the retina and the 
fibres from the macula pass back along the optic nerve until they 
come to what is known as the chiasm, where the various fibres from 
the eye decussate, in that the fibres from the inner half of each eye 
cross to the opposite side, whereas those of the outer half of each 
pass to the same side, as is shown in Fig. 136. After the optic 
tracts have been formed by this (partial) decussation each one 
winds around the corresponding cms cerebri, and terminates in 
two roots upon the corpora geniculata externa and interna and 
upon the posterior part of the optic thalamus. These parts are 
known as the primary optic centres. After leaving them the 
fibres pass backward into the posterior part of the posterior limb 
of the internal capsule and thence to the cortex, rise in a fan 
shape, pass outside the tip of the lateral ventricle, and reach the 
secondary or true optical centre in the lower part of the median 
aspect of the occipital lobe. (See Fig. 137.) 



378 



THE EYE 



Hemianopsia. — As lesions of the nervous centres frequently 
produce partial or complete blindness, it is of importance, first, 



£e/t Eye 



Visu^Fiela , 




'Pitai 



Lobe 



RiO 1 ^ 



Fig. 136. — The visual tract. The result of a lesion anywhere between the 
chiasm and the cuneus is to produce homonymous hemianopsia. H. Lesion at 
chiasm causing bilateral temporal hemianopsia. N. Lesion at chiasm causing 
unilateral nasal hemianopsia. T. Lesion at chiasm causing unilateral temporal 
hemianopsia. SN. Substantia nigra of crus. L. Lemniscus in crus. RN. 
Red nucleus. III. Third nerves. P, Q, R, S, U. Lesions in the occipital lobe 
and in front of it, producing left homonymous lateral hemianopsia. 



CHANGES IN THE ACUITY OF VISION 



379 



that the presence of partial blindness should be discovered, 
and, second, that the lesion causing it should be located. Aside 
from general failure of vision due to changes in the retina or optic 
nerve we have in many cases of nervous disease a condition called 
hemianopsia or partial or complete blindness of one-half of the 
retina. Usually hemianopsia is bilateral — that is, in both eyes; 
and it is usually homonymous — that is, on the same side of each 
eye; or, in other words, if it is in the outer half of the left eye, it 
will be in the inner half of the right eye. If this is the case, it 
produces right bilateral homonymous hemianopsia. If the outer 



LEFT VISUAL FIELD. RIGHT VISUAL FIELD. 

Fixation Point Fixation Point . 




(Oliver.) 



half of each eye is blind, this produces binasal hemianopsia; if 
the blindness is found in the nasal side of both eyes, it produces 
bitemporal hemianopsia. It must be remembered, that blindness 
of either visual field is due to disease of the fibres supplying the 
opposite side of the retina, as is shown in Fig. 132. 

The presence of hemianopsia in any form is determined by the 
following method of examination: The patient is placed with the 
back to the light and one eye is covered while the other is lixed upon 
the centre of the physician's face, which should be two feet away. 
The finger of the physician is now moved to the left and right as far 



3 8o 



THE EYE 



as the patient can see it, the head and the eyeball of the patient 
remaining fixed. If the eye fails to see the finger when but a little 
distance to one side or the other of the fixation point, hemianopsia 
is present. 

We measure the field of vision more accurately by means of what 
is known as a perimeter, which is a semicircular metal band which 
revolves upon its middle point, being capable therefore of describing 
a hemisphere in space. This arc is divided into degrees marked on 
it from o° to 90 and at the centre of it is placed the eye which is to 
be examined, which eye finds its fixation point in the centre of the 




Fig. 138. — Chart of visual field of right eye. 



semicircle. A small piece of white paper is now moved along the 
metal arc on its inner surface, from the extremity and toward the 
centre, until it comes into view, when the physician notes the 
number of degrees at which the object is seen and marks it on a 
chart (Fig. 133). The area of the normal field is well seen in this 
figure. 

Let us suppose that on using the tests just described we find left 
lateral homonymous hemianopsia — that is, blindness in the visual 
field, as shown in Fig. 134. This signifies that the patient has a 
lesion somewhere in the right visual tract back of the chiasm, 
either in the cuneus, in the occipital lobe, in the optic radiations, 



CHANGES IN THE ACUITY OF VISION 



38l 



in the internal capsule, in the primary optic centres, or in the 
optic tract. Fig. 131 shows the sites of these lesions and why they 
cause left homonymous hemianopsia. 




Fig. 139. — Left homonymous hemianopsia from a case of gunshot wound, 
with suspected lesion of the right cuneus. (de Schweinitz.) 




180 360 



210 




330 



270 270 

Fig. 140.— Bitemporal hemianopsia from a case of acromegaly, (de Schweinitz.) 

Supposing, on the other hand, that instead of left homonymous 
hemianopsia we find bitemporal hemianopsia (see Fig. 135), this 
indicates that the patient has a lesion of the optic tracts in the 
crossing fibres in the middle of the chiasm (see H in Fig. 131); 
or if binasal hemianopsia, that he has a lesion on both sides of the 
chiasm or one on the outer side of each optic nerve. This is a very 
rare lesion. 



;so 



3 82 



THE EYE 



Hemianopsia of the homonymous form is very rarely found in 
hysteria, generally in association with hysterical hemianesthesia, 
in which condition the conjunctiva is usually anesthetic, thereby 
differing from the condition of the conjunctiva of persons suffering 
from hemianesthesia of an organic origin. 

Visual Color Fields. — In some cases in place of hemianopsia we 
have simply an alteration in the visual fields for color. It will be 
remembered that the boundaries of the power of the clear per- 
ception of colors are not identical with the boundary for white 




WHITE 

blue 

RED 

GREEN 



Fig. 141. — Chart of visual field of left eye. (Landolt.) 



light, nor are they identical with one another. Passing from the 
periphery toward the centre of the visual field in ordinary daylight 
we find that blue is the color first seen, its boundary being almost 
as great as that of white. After blue come yellow, orange, red, 
and finally green. The blue, red, and green being the most impor- 
tant colors; their boundaries are shown in Fig. 136. These fields 
are determined by means of small pieces of colored paper passed 
around the perimeter in the manner already described. 

The alteration of the visual field for colors is called, if so changed, 
homonymous hemidyschromatopsia, and the lesion producing it is 



VISUAL COLOR FIELDS 



383 



situated in the cortex of the occipital lobe; while if the colors are 
indistinguishable, it is called hemiachromatopsia. This site of the 
lesion has recently been denied. 

The transposition of the visual fields for color is usually a symp- 
tom of hysteria, and, as a rule, the red field takes the place of the 
blue, and vice versa. The fields for all the colors are also markedly 
narrowed in hysteria. This transposition, rather than loss of color 
sense, helps us sometimes to a distinction between the ocular 
symptoms of hysteria and those of true tabes dorsalis, a distinction 
which is of great importance, yet one which is often exceedingly 
difficult, save for these and two other symptoms, namely, that in 
hysteria the knee-jerks are usually preserved and the Argyll- 
Robertson pupil is not seen. The following table from Charcot's 
lectures for 1888- 1889 summarizes these differential points: 





Tabes. 


Hysteria. 


Motor apparatus of the 


Paralysis from lesion of a motor 


1. 


Sometimes associated paralysis. 


eye. 


nerve of the eye (bulbar or per- 


2 


Blepharospasm. 




ipheral) ; consequent diplopia. 


3. 


Monocular diplopia ; micropsia 
and macropsia. 


Pupillary disturbances. 


Argyll-Robertson pupil. 






Optic disk. 


Atrophy. 






Symptoms due to affec- 


1. Irregular concentric contrac- 


1. 


Regular concentric contraction 


tions of the optic nerve 


tion of the visual fields. 




of the visual fields. 


or visual centres. 


2. Tabetic achromatopsia or dys- 


2. 


Dyschromatopsia from simple 




chromatopsia, affecting first 




contraction of the visual fields 




green and red, yellow and blue 




for colors. Frequently percep- 




being preserved to the last. 




tion of red alone persists. 




3. Progressive blindness. 


3. 


Transitory amblyopia or amau- 
rosis. 



It must not be forgotten that patients often have, in distinction 
from distorted images, visions or flames of light or bright sparks 
before the eyes, or in their place dark spots called muscce volitantes. 
Often the visions are the prodromes of an attack of migraine or of 
an epileptic seizure. In the case of spots of light or stars, we usually 
find them as a result of severe indigestion, and the dark spots may 
arise from the same causes. Muscae volitantes may also be due to 
small particles of mucus floating over the cornea, or to small 
floating bodies in the vitreous. 

Partial or complete blindness is sometimes seen in cases which 
are under the influence of a drug, as, for example, quinine or other 
drugs; and sometimes partial or complete blindness results from 
uremia (uremic amaurosis). As a rule, it does not occur as a single 
symptom, but follows an attack of acute uremic manifestation— 
that is, it is found after a convulsion or period of coma has passed 



384 THE EYE 

by. As a rule, nothing abnormal is found in the eye to account for 
it, and the pupillary reflexes are intact. The effect of the poison 
in the blood is, therefore, exercised upon the optical centres, prob- 
ably in the occipital lobe. Sight is usually regained in these cases 
in a few days. 

The Optic Nerve and the Ophthalmoscope. — There still remain 
to be considered the diagnostic indications afforded us by the optic 
nerve. Before taking up this subject mention must be made of the 
manner of using the ophthalmoscope. 

The patient is to be seated in a darkened room, and by his side, 
at the level of the eye to be examined and far enough back of him 
for his face to be in shadow, should be placed a lamp, or, if gas can 
be had, an Argand burner. The physician now seats himself, if 
the right eye is to be observed, at the right side of his patient, and 
takes a chair slightly higher than that of the patient. The ophthal- 
moscope is now taken in the right hand and held in such a position 
that the concavity of the physician's brow fits over the convexity 
of the instrument. The eye of the physician is so placed that he 
can readily see through the aperture in the centre of the ophthal- 
moscope, and by means of the concave mirror on the face of the 
instrument he reflects the light into the eye through the pupil. 
The patient must not look into the ophthalmoscope, but to one 
side, and his vision should be directly distant and accommodation 
so far as possible relaxed. If the examiner is not skilled in the use 
of the ophthalmoscope and the result of the examination is of 
great importance in the diagnosis of the case, it is justifiable to use 
homatropine to dilate the pupil and prevent the alterations of 
accommodation by paralyzing this function. The ophthalmoscope 
and the head of the physician are now approached as closely as 
possible to the eye of the patient, the angle of the two heads being 
as nearly as possible identical, as shown in Fig. 137. If the light 
be now directed slightly toward the nasal side of the eye, the optic 
nerve will be seen, or in its stead a retinal bloodvessel will be seen 
across the field of vision, and this should be traced along its course 
to its origin in the papilla. If the patient or the physician is short- 
sighted (myopic) , the ophthalmoscope must be adjusted to correct 
this error by placing over the aperture a concave lens; but if 
ordinary degrees of far-sightedness (hypermetropia) are present, 
the use of a convex lens is not necessary, because the accom- 
modation of the eye makes up for the error in refraction. If the 
hypermetropia is so great that accommodation cannot overcome it, 
then a convex lens must be used. The view of the eye which is 
obtained ordinarily by a beginner is clouded, not because of myopia 
or hypermetropia, but because the physician has not as yet learned 
to relax his accommodation in making the examination. A concave 
glass usually remedies this. 



THE OPTIC NERVE AND THE OPHTHALMOSCOPE 



38s 



In health the optic nerve appears as a nearly round or slightly 
oval disk, situated somewhat to the nasal side of the eye, and vary- 
ing in color from grayish pink to red, the centre being whiter and the 
nasal half the darkest part. Around the papilla are seen two rings, 
the outer one darker and generally incomplete or absent, while the 
inner one is a faint white stripe, which becomes more marked as 
the patient grows older. The first is called choroidal ring, and 
represents the edge of the choroidal coat of the eye where it is 
pierced by the nerve. The second is the scleral ring, which is the 




Fig. 1 42. —Relative position of physician and patient while employing the 
direct method. (Norris and Oliver.) 



edge of the sclerotic coat. The centre of the optic papilla may be 
even with the surface or cupped, and may be stippled or dotted 
in appearance. The retinal arteries emerge from this central spot, 
and the chief venous trunks empty into it. Generally one arterial 
and one venous stream pass up and a similar one downward, and 
both soon bifurcate, afterward still further dividing. The arteries 
are distinguished by their bright-red hue, while the veins are darker 
in color. The veins are about one-third larger than the arteries. 
A bright stripe due to an optical delusion seems to divide each 
vessel longitudinally into two parts. The arteries of the normal 
25 



386 THE EYE 

eye do not pulsate, but pulsation of the veins is quite common. 
It must be remembered that the appearance of the papilla and of 
the bloodvessels as they leave it varies very greatly within perfectly 
physiological limits. As already stated, the cupping of the papilla 
may be quite deep or quite shallow, and the bloodvessels may 
divide, as already described, or divide in the papilla into four 
branches. The veins are usually more tortuous than the arteries. 
The retina is practically transparent, so that the underlying 
choroid is seen. In persons with a dark skin the retina has a 
grayish hue in the neighborhood of the papilla, which is most 
marked on its nasal side and is slightly streaked. 

To the outer side of the papilla, slightly below the horizontal 
meridian, is the macula lutea, or yellow spot, which is about the size 
of the end of the optic nerve, but darker in color, somewhat granular 
and devoid of any retinal vessel. It is the point of the eye-ground 
in which direct vision is best developed. In its centre is a bright 
spot, the fovea centralis. As a person grows older these clear dis- 
tinctions vanish, and the macula lutea is to be distinguished from 
the surrounding eye-ground only by its darker hue and the absence 
of vessels. The macula is difficult to see, because, as the light falls 
on it, the pupil at once contracts, unless the pupil is dilated by a 
mydriatic. 

The red glare produced by throwing the light into the eye by the 
ophthalmoscope is due to reflection from the bloodvessels of the 
choroid coat. 

The pathological significance of alterations in these normal 
appearances is very great. 

Optic Neuritis. — In the presence of optic neuritis we find the end 
of the optic nerve red and its edges irregular and obscure, or, if the 
morbid condition is further advanced, the nerve head looks pro- 
truding or mound-like and the arteries going to it are smaller than 
normal and partly concealed, while the veins are enlarged and 
tortuous. Flame- shaped hemorrhages may be seen in the papillary 
region or near it. 

Optic neuritis depends upon intra-orbital or intracranial disease, 
although, if the process is not marked, it may be due to hyper- 
metropic astigmatism. Vision is often unaffected, but if the lesion 
be in the cerebellum, sudden blindness may come on. 

As some differences of opinion exist as to the various forms of 
neuritis of the optic nerve, the term papillitis is often used to signify 
all the forms of optic neuritis which we meet with, or in other cases 
is spoken of as " choked disk." Papillitis is more commonly the 
result of brain tumor than of any other intracranial lesion, and, 
again, it is much more common in lesions of the cerebellum than in 
tumors elsewhere in the brain. Another fairly common cause of 
papillitis is meningeal inflammation, particularly about the base 



OPTIC NEURITIS 



387 



of the brain, and tuberculous meningitis is very prone to produce 
it. Cerebral abscess may also cause this change in the optic nerve. 
In addition to the cranial causes of papillitis, we have acute 
febrile disorders, syphilis, toxemias from lead and alcohol, rheuma- 
tism, and anemia. Sometimes, however, they produce an acute 
or chronic retrobulbar neuritis. There is nearly always in such 
cases a large central scotoma, which causes a failure to recognize 
color, as, for example, green or red. Sometimes the patient realizes 
the failure of his vision, which may be impaired otherwise than by 
disorder of the color sense. In other cases he fails to do so until 



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Fig. 143. — Upper curve frequency of tabes. Middle curve frequency of 
severe ocular symptoms. Lower curve frequency of atrophy of the optic nerve. 
(Berger.) 



his eyes are examined. The chronic form of retrobulbar neuritis 
is generally the result of the excessive use of tobacco and alcohol, 
and produces what is called tobacco amblyopia or toxic amblyopia, 
with failure of vision from these causes. In such cases there is a 
central scotoma between the macula and the optic nerve where 
the senses of red and green are lost. The ophthalmoscope may 
reveal, in such cases, discoloration of the disk and a triangular 
spot of atrophy in the outer and lower part of it. Supposing. 
however, on using the ophthalmoscope we find in place of a papil- 
litis an atrophied state of the nerve, in which, if the disease be 
young, the nerve ending looks gray and the outline of the disk is 



THE EYE 

sharp, or, if it be well advanced, the edges appear hazy, the arteries 
contracted, and the veins large and tortuous, while the disk is 
quite white. This primary or gray form of atrophy is most typically 
seen in the optic nerve lesion of locomotor ataxia, and so is often 
called tabetic atrophy. About 34 per cent, of all tabetics suffer 
from this change. Again, it is seen in cases of paretic dementia 
somewhat less frequently. Optic atrophy is often seen in cases of 
disseminated sclerosis. Because of the fact that gray atrophy of 
the nerve is one of the earliest signs of locomotor ataxia, in some 
cases it is a valuable one in the diagnosis of this grave disorder, 
separating it from pseudotabes due to ordinary peripheral neuritis. 
The diagram (Fig. 143) on page 387, taken from de Schweinitz's 
article on this subject, shows the relation between age, severe 
ocular symptoms, and atrophy of the optic nerve. 

The more advanced forms of optic atrophy with a hazy outline of 
the disk usually result from diseases in the optic centres or in the 
nerve itself. Thus there may be present a tumor pressing on the 
chiasm or optic tracts. 

Retinitis. — If, on the use of the ophthalmoscope, we find that 
there is a faint haziness of the retina, that whitish streaks are seen 
in it which may be bluish-gray or yellowish in hue, that the blood- 
vessels are tortuous and minute vessels are easily seen because of 
their enlargement, that hemorrhagic exudations of a flame-like 
character are present, that dark pigmented spots show where 
previous hemorrhages have been, and, finally, that the head of the 
optic nerve is not clearly outlined, we have the picture of retinitis. 
Generally, in association with these signs, we find, as subjective 
symptoms, changes in the visual field, a distorted vision, so that 
straight lines appear bent inward or outward, and there are pain 
and fear of light. If, in addition to these symptoms, the vitreous 
humor is opaque, syphilis may be present, and the iris may give 
evidence of iritis. Where the hemorrhages are very manifest and 
profuse (hemorrhagic retinitis), the cause may be disease of the 
heart and bloodvessels. 

By far the most important of these forms of retinitis from a 
diagnostic standpoint is what is known as albuminuric retinitis, or 
that due to parenchymatous nephritis. Here, in addition to the 
flame-like hemorrhagic areas, we find irregular spatterings of white 
which may be star-shaped. If the retinitis be due to chronic 
B right's disease, the prognosis is very bad, death occurring in a 
year in 50 per cent, of the cases, whereas not 20 per cent, five more 
than two years. The importance of the discovery of such changes 
is that by it the first suspicion of renal trouble is aroused. This 
sign is of the greatest value in pregnancy, in which the ultimate 
prognosis is not so grave. Retinitis also sometimes results from 
diabetes. 



.RETINITIS 389 

Hemorrhages into the retina without retinitis are usually the 
result of septicemia, ulcerative endocarditis, hemophilia, diabetes, 
gout, and malarial fever of a severe type. They are also seen in 
cases of great cardiac hypertrophy with stenosis, and after suffo- 
cation. 

Ophthalmoscopic evidence of general arterial disease and chronic 
contracted kidney not infrequently is manifested by edema of the 
retina and retinal hemorrhages; but an early sign is the influence 
of the arterial pressure on the venous blood streams of the retina, 
where artery and vein cross one another. There may be simply 
inequality in the caliber of artery and vein, or the vein may be 
somewhat displaced, where it lies beneath the artery, in the direc- 
tion of the arterial circulation, and its flow obstructed. In advanced 
cases the vein is greatly narrowed where the artery crosses it, and 
distended on its peripheral side. When these appearances are 
well studied, they are exceedingly suggestive of early arterial 
changes. Changes of this character, as the author can testify from 
studies made with Dr. de Schweinitz, are of serious prognostic 
import and may be the forerunners of intracranial extravasations. 



CHAPTER XIV. 
CHILLS, FEVERS, AND SUBNORMAL TEMPERATURES. 

Chills — The methods of taking the temperature — The significance of fever — 
The febrile movements of various diseases. 

CHILL. 

A chill is of very considerable diagnostic importance when 
observed by the physician, or even when reported as having 
occurred in the immediate history of the patient. It may follow 
prolonged exposure to cold, without subsequent development of 
disease, or be a precursor of some acute malady. Often it is an 
early symptom of the onset or one of the acute infectious diseases, 
such as croupous pneumonia, erysipelas, or scarlet fever. In 
other instances it is a symptom of the development of a purulent 
or pyemic process. When chills recur repeatedly they may be due 
to malarial infection, in which case they may be controlled by 
using quinine; as a result of suppuration and general pyemia; and 
finally, they may indicate tuberculosis or ulcerative endocarditis. 
In some cases of typhoid fever a chill ushers in the attack, and chills 
may repeatedly occur without apparent cause, so that the disease 
may be very like remittent malarial fever. (See Figs. 144 and 145.) 



FEVER. 

Fever is that state of the human body in which its temperature 
is raised above the normal limit, or 98.8 ° F., but variations from 
9 7. 8° to 99. 5° may occur without indicating disease. From 99.5 ° 
to 100. 4 the temperature is spoken of as subfebrile, from 100.4 
to 1 01. 3 as mildly febrile, while the term decidedly febrile is 
applied to temperatures varying from 103. i° to 105 °. Hyper- 
pyrexia is a term applied to a febrile movement in which the 
temperature rises as high as 106 °. Cases are on record of a tem- 
perature of 115 or even more. 

The method of taking the temperature consists in placing a self- 
registering clinical thermometer in the mouth under the edge of 
the tongue, the lips being then closed tightly about its stem; or of 
inserting it in the axilla, the hand and arm being then placed across 



FEVER 



391 



101° 

100° 

99° 

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Day of Dis. 

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1 : : Va.v 



392 



CHILLS, FEVERS, AND SUBNORMAL TEMPERATURES 



the patient's chest or epigastrium, so as to cause the axillary 
tissues to be in close contact with the bulb of the thermometer. 
Before the thermometer is placed in the axilla this space should be 
carefully wiped dry, since if perspiration is present its evaporation 
will so chill the thermometer that a false record will be made by 
the index. Sometimes the temperature of the patient is taken by 
inserting the thermometer into the rectum; and, if this is done, 
the bulb should be passed well inside the external sphincter. 
Rarely the temperature is taken in the vagina. In the rectum and 



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Fig. 145. — "Chills and fever" in course of typhoid fever. 



vagina the normal temperature is about i° to 1.5 degrees higher 
than in the axilla. In fat children the fold in the groin gives equally 
reliable results with those obtained by inserting the thermometer 
in the rectum, provided it is wiped free of perspiration. 

The precautions to be taken in all cases in which a thermometer 
is used, in addition to those named, is to have a thermometer which 
is accurate, and to be sure that there is no acute or chronic inflam- 
matory process present which will produce local heat, and so give 
an erroneous impression as to the actual temperature of the entire 
body. This is particularly apt to be the case in diseases of the 



FEVER 393 

mouth in children: thus, stomatitis may raise the local temperature 
from i° to 2°. Hot liquids, if taken into the mouth just previous 
to or during the time at which the thermometer is inserted, will 
so raise the temperature of the local tissues as to make the ther- 
mometer register several degrees above normal, and low records 
may be produced by cold liquids or ice held in the mouth. This 
subject has been studied by Lazarus-Barlow, who asserts that the 
effects of hot objects taken into the mouth last much longer than do 
those produced by cold, and that a mouth temperature should never 
be taken within one hour of the time that any hot food is ingested. 
He even shows that holding the mouth open for some time renders 
a true estimate of the body heat impossible, and advises that the 
temperature should never be taken in the mouth if it were 
possible to take it elsewhere. 

Febrile movements are generally associated with a dry, hot skin, 
but sometimes with a cold, wet skin. The latter condition is of evil 
significance, as a rule, and should be remedied if possible. 

The Significance of Fever. — The significance of fever is great. 
It always shows the presence of an ailment sufficiently severe to 
make it wise for the physician to order the patient to bed until 
the fever abates or until he can surely determine its cause. The 
significance of a raised bodily temperature from a physiological 
point of view is that the nervous centres governing heat production 
and heat dissipation are disturbed by some substance circulating 
in the blood or by reflex irritation, or perhaps by both. The danger 
of very high fever is that it may cause morbid changes in the 
protoplasm of the heart or in the vital centres at the base of the 
brain, but the danger of ordinary febrile temperatures has been 
greatly exaggerated. Indeed, in some cases moderate fever prob- 
ably aids the body in combating or, rather, conquering the disease 
which has attacked it. This may occur in three ways, namely, 
by producing a temperature less favorable to the growth of certain 
disease germs than is the bodily temperature in health; by increas- 
ing cellular activity it may increase phagocytosis and the develop- 
ment of antitoxic materials; and, finally, by virtue of the increased 
temperature, the effects of poisons may be rendered nil. This is 
the case, for example, in regard to the drug digitalis, which will 
rarely produce its ordinary effects on the heart when well-marked 
fever is present. Another point of importance in this connection 
is, that the duration of fever has more to do with its importance 
as a symptom than has its degree, for a temperature of 105 ° for a 
few hours may be borne with impunity, whereas one of 103 ° for 
many days cannot fail to produce evil effects. 

Fever in children does not possess nearly as grave significance as 
it does in adults, for children often develop high temperatures from 
slight causes and have speedy recoveries. The balance of their 



394 CHILLS, FEVERS, AND SUBNORMAL TEMPERATURES 

heat-mechanism is easily upset. The older the patient the greater 
the significance of fever, and a rise of 2° or 3 ° in a man of sixty 
years is more alarming than one of 4 or 5 ° in a child of five or 
six years. 

When fever is not due to a distinct pathological change in some 
part of the body, generally of an inflammatory kind, it may arise 
from a mild irritation of a mucous membrane, as when a catarrhal 
condition is set up. Such fevers are seen in cases of mild gastro- 
intestinal catarrh in children after the ingestion of bad food or 
exposure to cold. Sometimes fever apparently arises as the result 
of the reflex irritation produced by difficult teething (see chapter 
on the Mouth and Tongue), although in many instances the fever 
of dentition depends upon a more or less closely related, but over- 
looked, gastric catarrh. Sometimes after a urethral sound or 
catheter has been passed into the urethra of a man, in the 
course of a few minutes or hours he develops a severe chill, 
followed by a fever which may be quite high, but which rarely 
lasts long. 

Fever in Infectious Diseases. 1 — Nearly all infectious diseases 
are ushered in by the development of fever of greater or less degree, 
and this is particularly true of the exanthemata. Inquiry should, 
therefore, be made by the physician as to the previous history of 
infectious disease. If one or more of the eruptive fevers have 
already been present, they can usually be excluded from the 
diagnosis of the illness present at the time of the visit. If, on the 
other hand, there is a history of pulmonary tuberculosis or acute 
articular rheumatism, this may indicate that another attack is 
coming on. 

In typhoid fever the febrile movement is very characteristic in 
some cases, although in many instances it does not follow the 
description laid down in text-books. After several days of general 
wretchedness the patient develops a slight fever of from ioo° in 
the morning to 101 at night, and this temperature progressively 
rises so that the next morning it may be 101 and that night 102 °, 
the next morning 102 °, that night 103 °, and so on until the morning 
temperature may be 103 ° and the evening temperature 104 or 
rarely 105 °. The fever usually reaches its acme by the end of the 
first week or ten days, and then for another week remains prac- 
tically unchanged, there being a morning fall and evening rise of 
an almost equal extent. Toward the end of the third week, or 
sometimes earlier or later, according to the severity of the attack, 
the morning remissions become more marked, and then the evening 
rises fail to reach their former height. Often these marked morning 
remissions are the first indication of the tendency to recovery. 

1 In this connection the student should also read that part of the chapter on 
the Skin devoted to the consideration of the eruptive infectious diseases. 



FEVER 



395 



Very high evening temperatures are indicative of a severe attack, 
but are not so indicative of serious illness as are high temperatures 
in the morning. After the second or third week, in a moderately 
severe case, the temperature falls gradually until by the twenty- 
first or twenty-eighth day it usually reaches the normal. In very 
rare cases the temperature speedily reaches its acme at the very 
beginning of the disease, and then passes through the course 
already described. Such cases are generally prolonged, but may 
in some instances end by the fourteenth day. In other instances 
the development of high fever in the early stages of enteric fever, 
associated with severe general symptoms, is indicative of a short 
attack rather than a prolonged and severe one. 

As the end of the disease approaches the morning temperature 
may be practically normal and the evening temperatures be as 
high as before. This is a sign of convalescence. It is called the 
"period of steep curves," the "period of ambiguity" or the "time 
of changing fortunes." 



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Fig. 146. — Showing recrudescence of fever in a case of typhoid fever. 

Sudden falls of temperature during the course of typhoid fever 
are nearly always of grave import. The most common cause of 
such a sudden fall is an intestinal hemorrhage, and the fall may 
occur sometimes before the blood appears in the stools. In other 
cases such a fall is an evidence of intestinal perforation. The 
other causes of a sudden fall are severe nose-bleed, or hemorrhage 
of any form; as, for example, that occurring in connection with 
abortion. Sometimes, too, without any of these causes, the tem- 
perature falls very rapidly, and the patient goes into collapse. 
Such cases are very grave and the prognosis is unfavorable. 

A recrudescence or return of the fever, in which it rises quite 
rapidly to a point as high or higher than at any time during the 
attack, occurs in some persons who during the stage of convales- 
cence from typhoid fever, eat heartily too soon, or arc excited by 



396 CHILLS, FEVERS, AND SUBNORMAL TEMPERATURES 









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FEVER 397 

the visit of a friend. Such rises are but temporary (Fig. 147). 
More rarely, possibly, as a result of getting out of bed too 
soon, or bad feeding, or other causes, a true relapse takes place, 
and the disease runs a second course, which is usually, but not 
always, of a shorter and milder character than the first attack. 
Sometimes a mild, irritative fever, perhaps due to anemia, persists 
for some weeks, but the physician should not rest content with a 
belief that anemia is the cause until he has excluded all possibility 
of there being pulmonary, pleural, acute renal, or bone disease, as 
these conditions very commonly ensue as sequels of typhoid fever. 
In other instances, after the morning temperature has reached 
normal, the evening temperature remains pyretic for a number of 
days, and this may persist for some time. In a number of instances 
I have known the use of strychnine in full doses, at this period of 
the disease, to produce ranges in temperature, which ceased as soon 
as the use of the drug was stopped. 

If the temperature in the course of a case of typhoid fever rises 
as high as 107 or 108 , the prognosis at once becomes very grave. 

Very rarely enteric infection, so called, runs its entire course 
without any fever. Fisk, of Denver, and others have seen such 
cases, and the author had five of them at St. Agnes' Hospital in 
one term of service. 

Striimpell asserts that as a rare occurrence the fever in this 
disease may become intermittent, being normal in the morning 
and as high as 104 at night during almost the entire illness. 

The association of such a temperature curve as just described 
with the other characteristic signs of typhoid fever, as, for example, 
the development of the rose rash on the chest and abdomen, on or 
about the seventh to ninth day (chapter on the Skin), the ochre- 
colored, loose stools, the peculiar stupid, drowsy appearance of the 
face, the Widal test, and in some cases the peculiar typhoid odor 
about the patient, all make the diagnosis certain. 

Irregular forms of malarial fever, particularly those forms due 
to infection by the estivo-autumnal parasite, may closely resemble 
typhoid fever. In many instances such cases are diagnosticated 
as typhoid fever, and probably some cases of true typhoid fever 
are thought to be malarial fever. The following differential table, 
drawn up by Thayer, is of interest in this connection. There is 
no such disease as typhomalarial fever, although there is no doubt, 
whatever, that pure typhoid infection may result in the production 
of a fever which closely follows the remittent and intermittent 
malarial types, and which is often associated with so much gastric 
disturbance and vomiting, and so lacking in the more prominent 
typhoid symptoms usually seen, that the picture of remittent 
malarial fever is clear, while the true picture of typhoid fever is 
clouded. 



398 



CHILLS, FEVERS, AND SUBNORMAL TEMPERATURES 



Remittent Fever. 
Onset generally intermittent. 
Irregular remissions. 



The temperature may arrive at 40° C. (104° 
F.) within twenty-four hours. 

Remittent Fever. 

Headache rare in the beginning ; of a neu- 
ralgic character, pulsating, variable in its 
position and intensity. Sclera subicteric from 
the onset. 

The apathetic expression of the face, the dry- 
ness of the tongue, and sordes upon the teeth 
are not very marked. 

Breath foul. 

The delirium may come on in the early days ; 
it is recurrent, but changes with the exacerba- 
tions of temperature and other symptoms, and 
may give way to grave symptoms related to 
other organs. 

If there be pulmonary congestion, the cough 
and other symptoms come on suddenly; the 
areas affected change from one to the other 
lobe or lung, and may disappear and reappear 
again with varying intensity ; dyspnoea is very 
pronounced ; circulatory disturbances are 
marked, even syncope. 

There are usually restlessness and anxiety 
(jactitatio corporis:. 

Peculiar grayish color of skin ; sometimes a 
slight jaundice. 

Herpes common. 

Anaemia more or less marked early in the 
course. 



No characteristic exanthem 
uncommon. 



urticaria not 



At times there may be transient tympanites 
or ileo-csecal gurgling ; they are but slightly 
pronounced and paroxysmal ; diarrhoea is 
slight or absent, and has not the characters of 
that in typhoid fever. 

No distinct course. 

Urine high-colored; may show a trace of 
bile ; Ehrlich's diazo-reaction rarely present. 

Blood shows no leucocytosis ; eosinophiles 
not notably diminished ; serum does not cause 
agglomeration of typhoid bacilli (Pfeiffer, 
Durham, and Widal) ; malarial parasites and 
pigmented leucocytes present. 

Fever disappears under quinine. 

Is an endemic disease occurring particularly 
in rural districts ; rarely epidemic. 



Typhoid Fever. 

Onset gradual and progressive. 

Regular, though very slight morning remis- 
sions with evening exacerbations of tempera- 
ture. 

The temperature does not reach 40° C. 
(104° F.) before the third or fourth day. 

Typhoid Fever. 
Headache from the beginning, permanent, 
severe, frontal. Sclera white. 



These symptoms are well marked and pro- 
gressive. 

Breath has a peculiar mouse-like odor. 

Delirium appears only when the disease is 
well pronounced ; it is often persistent, and 
variable only in degree. 



Pulmonary congestion is gradual and per- 
sistent ; always hypostatic (the bases and dor- 
sal surfaces of the lungs) ; the dyspnoea is less 
pronounced and later in appeariug, depending 
more upon the abdominal conditions (tym- 
panites, etc.). 

There are usually relaxation, prostration, 
and stupor. 
No jaundice. 

Herpes rare. 

Anaemia absent, excepting in later stages. 

Characteristic roseola. 



Tympanites, gurgling, and diarrhoea appear 
slowly and may become well marked. 



Has a fairly characteristic course. 

Urine high-colored ; bile absent ; diazo-re- 
action present during the height of the process. 

Blood shows no leucocytes ; eosinophiles 
diminished or absent ; serum causes agglomer- 
ation of typhoid bacilli ; malarial parasites and 
pigment absent. 



Fever uninfluenced by quinine. 

Usually epidemic ; prevailing commonly in 
cities. 



Again, there can be no doubt that cases of true malarial infec- 
tion occur in which the symptoms so closely resemble those of 



FEVER 399 

typhoid fever that a purely clinical diagnosis is almost impossible, 
particularly if an epidemic of typhoid fever is in full swing at the 
time. Finally, there can also be no doubt that it is possible for the 
patient to have a double infection with the bacillus of Eberth and 
the plasmodium of Laveran, in which case, however, the malarial 
manifestations are usually dwarfed by the typhoid infection, and 
are only marked at the onset of the enteric fever and at its termin- 
ation. To this mixed infection the term typhomalarial fever may 
be correctly applied to indicate not a separate disease, but a double 
infection. Etymologically, this term might also -be used to define 
a condition of malarial fever in which, because of profound debility, 
the patient is in a typhoid state — that is, in a condition of which 
typhoid fever is a type. Practically, however, it should be dis- 
carded or limited in its use to the double infection just described. 
(For Malarial Fever, see page 404.) 

The febrile movement and other symptoms of enteric fever are 
often imitated very closely by those of ulcerative endocarditis. In 
addition to an irregular fever, there may be diarrhea, parotitis, 
stupor, and progressive feebleness in both diseases. An examina- 
tion of the heart may reveal the presence of endocardial murmurs, 
which in association with signs of sepsis, or the existence of some 
focus of infection, such as a wound, a septic process, or the fact 
that the patient is in the puerperium, will render a diagnosis 
possible. (See also page 406.) 

The differential diagnosis of acute tuberculosis from typhoid 
fever may be quite difficult in certain cases. When the symptoms 
of the two conditions are compared this is not difficult to believe,, 
for we often have in both diseases headache, epistaxis, a very 
similar temperature chart, and a feeble pulse, while there may be 
in both conditions an eruption on the skin, which rather tends to 
confuse the physician than to aid him. Again, the delirium in 
each case is very similar, and the facial expression of the patient 
in both diseases is apathetic. Even the respiratory sounds in 
both diseases in their early stage may be apparently only those 
of a moderate bronchitis; and, finally, abdominal swelling, tym- 
panites, and meteorism may occur in both maladies. Under these 
circumstances the hereditary and recent history of the patient 
may be of much value, as showing a tendency or exposure to 
tuberculosis on the one hand, or exposure to typhoid infection on 
the other. Again, if it be typhoid fever, the spleen on percussion 
is nearly always found to be enlarged. Then, too, the lesions in 
the lungs of a typhoid fever patient are generally at the bases. 
while in tuberculosis they are oftener at the apices. The stools 
may be loose in both diseases, but in typhoid fever they are apt 
to be ochre-colored; and, again, in tuberculosis the loss of flesh is 
often exceedingly rapid, and profuse sweats and high fever are 



4-00 CHILLS, FEVERS, AND SUBNORMAL TEMPERATURES 

frequently seen. The mental apathy in typhoid fever is more 
marked, as a rule, than it is in tuberculosis. The rinding of Widal's 
reaction in the blood, or the discovery of the bacillus of Eberth 
in the feces and the presence of the diazo-reaction in the urine, 
would, of course, indicate typhoid fever. Finally, careful and 
repeated examinations of the chest will usually, in the course of 
the disease, demonstrate the presence of tuberculosis of the thoracic 
or abdominal organs, if this be the cause of the illness. It seems 
hardly necessary to state that if any expectoration exists the 
sputum is to be carefully examined for tubercle bacilli in all doubt- 
ful cases, but while their presence proves tuberculous infection 
to be present, their absence does not prove the absence of this 
infection. 

An irregular fever with muscular pains and a great deal of dis- 
comfort in the belly, the case simulating typhoid fever, may occur 
in cases of trichiniasis . 

A febrile movement closely resembling that of typhoid fever, 
a resemblance which is increased by the association with it of 
headache, insomnia, and anorexia, may be Malta fever, a disease 
which can be excluded in the vast majority of cases if there is 
no history of exposure to the exciting cause in the island of Malta, 
although it is not to be forgotten that Malta fever has been met with 
in Texas and in persons returning from Porto Rico and elsewhere 
during the last few years. Sometimes it may be confused with 
relapsing fever, except for the longer febrile movement. Thus, after 
three or four weeks of illness convalescence seems to be established, 
and the temperature falls, but in a few days all the symptoms 
return with even greater vehemence than before. Such relapses 
may occur again and again. Violent pain in the joints on moving 
the body is often present. In doubtful cases the agglutination 
test with the blood may be performed, if it is possible to obtain 
cultures of the Bacillus melitensis. 

The temperature chart of typhus fever is so different from that 
of typhoid fever that it gives us a valuable differential point at 
the very beginning of the disease, for, after several days of languor, 
headache, and pain in the limbs, the fever suddenly springs on the 
patient, so that on the first night it may reach 105 ° F. Often 
it reaches 106 in a day or two, and while present is constant, the 
morning fall being very slight indeed. The development of the 
spots in a copious eruption on the third to the seventh day, which 
spots may develop into petechias before fading, or remain unchanged 
in appearance, the great exhaustion, the severity of the illness, 
and the sudden rise of temperature, followed by a constant fever, 
point to typhus fever. Finally, the conclusion of the febrile move- 
ment, in favorable cases by the end of the second week, by crisis 
or by^ajnore rapid fall of temperature than we are accustomed 



FEVER 



401 



to see in typhoid, all help to make the differential diagnosis, which 
is, however, in many cases very difficult or impossible in the early 
stages. Typhus fever is so rarely met with in the United States 
as to be excluded by its rarity in nearly every case. 

A modified form of typhus fever first described in this country by 
Brill (Brill's disease) is that in which the fever reaches its acme on 
the third or fourth day, averaging 103 ° to 104 . The rash appears 
on the fifth or sixth day and is maculopapular in type; not disap- 
pearing on pressure, not very profuse, rarely hemorrhagic, and dull 
in hue. The fever lasts twelve to fifteen days and ends by crisis. 
It does not seem to be contagious. A similar mild form in the Far 
East is called Manchurian fever, whereas the Tarbadillo fever, or 
typhus fever of Mexico, is often very severe. 

The temperature of relapsing fever nearly always rises suddenly 
at the beginning of the attack to from 103 ° to 105 °, and remains 
high with slight morning remissions from three to seven days, 
when it suddenly falls as by crisis to the normal or below it, after 
being on the preceding afternoon or evening unusually high. 
Sometimes it falls as low as 92 ° or 93 °. The patient now remains 
free from fever for from several days to two weeks, when with a 
sudden leap the fever and other symptoms of the first attack 
recur. A temperature of 105 ° to 106 in relapsing fever rarely 
indicates a grave outlook, as it does in typhoid. The only con- 
dition which resembles this temperature range of relapsing fever 
is intermittent malarial fever; but the great rarity of relapsing 
fever in America, the frequency of malarial fever in certain parts, 
the presence of the spirillum of Obermeier in the blood in relapsing 
fever, and the malarial germ in the blood of intermittent fever, all 
make the diagnosis possible. 



DAY OF 
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Fig. 148. — Chart of scarlet fever. 



In scarlet fever the temperature suddenly rises on the first day 
to 104 to 105 °, and still higher on the next day, and then remains 
constant as long as the eruption is on the skin in full development. 
Just as soon as the eruption begins to fade the temperature also 
falls, not by crisis, but by lysis; not so slowly as in typhoid fever. 
26 



4-02 



CHILLS, FEVERS, AND SUBNORMAL TEMPERATURES 



but far more slowly than in croupous pneumonia (Fig. 148). 
This arrest of the fever usually takes place in simple cases by the 
end of seven days; and if it persists longer, is probably due to 
some complication, such as otitis, or the "collar of brawn," due to 
enlarged cervical glands. The characteristic strawberry tongue, 
punctated rash and scarlet hue appearing on the first or second 
day, the pallor about the nose and mouth, the ultimate dermal 
desquamation, the violence of the onset of the symptoms, the sore 
throat, and the peculiar appearance of the skin, all complete the 
clinical picture, particularly if the symptoms occur in a child. 
(See chapter on the Skin.) 

In rare cases the fever in scarlatina is remarkably mild or almost 
absent, and these cases, as a rule, have a favorable prognosis. If 
the temperature be very high and persistent, on the other hand, the 
case is usually to be regarded as most grave. 




Fig. 149. — Showing initial fever with the subsequent fall and then a rise when 
the rash is well developed in a case of measles. Also shows an ending of the 
fever by crisis. 



In measles the fever at first rises sharply to 103 ° or thereabout, 
then falls to a little above normal, is slight for several days, and 
then markedly increases with the development of the eruption 
on the fourth day, often ranging as high as 104 or 105 °, at which 
point, with little variation, it remains for the two days during 
which the rash is well developed (Fig. 149). With the fading of 
the rash the temperature also falls by crisis. If fever persists to 
any extent, it is always due to some complicating cause other than 
the original disease; such a complication, for example, as a bron- 
chial or gastroduodenal catarrh or a catarrhal pneumonia. 

The fever of rotheln, if any occurs, is very seldom more than 
102 , and has no typical preliminary rise as has measles, so that 



FEVER 403 

the temperature chart of the disease may aid materially in a 
differential diagnosis. (See chapter on the Skin.) 

The febrile movement of smallpox is, with the exception of that 
of typhoid fever, the most characteristic of all the eruptive diseases. 
With a sudden onset of fever, pain in the back, severe headache, 
and malaise, the patient takes to his bed if possible, and his tem- 
perature if taken will be found speedily to rise even to 105 ° or more 
in some cases, and then falls back to almost normal for two or 
three days, during which time the eruption appears. In this way, 
therefore, the temperature chart of variola differs diametrically 
from that of the eruptive fevers so far discussed, for in these cases 
the fever rises with the appearance of the eruption, whereas in 
this instance the temperature falls with the appearance of the 
eruption. This lower temperature persists for several days, from 
\° to i° above normal until the ninth day of the disease or the 
sixth of the eruption, when with the change of the pocks from 
vesicles to pustules the temperature rises again in what is called 
the fever of suppuration, which lasts with greater or less per- 
sistence for at least a week, when it ends by lysis or a gradual fall. 
Excessively high fever of 108 is a sign of very grave import. 

The febrile movement of varicella, or chicken-pox, is usually of 
very short duration and of little severity; but it may reach pro- 
portions entirely out of consonance with the general systemic 
disturbance, which is usually very slight in previously healthy 
children. Thus, it may rise in children who are prone to active 
febrile movements to as high a point as 105 ° for a very brief period, 
and yet may not seem to render the child very ill. 

The temperature range seen in cases of erysipelas is quite typical. 
At the beginning of the attack the rise is quite prompt and sharp 
to 105 ° or 106 or even above this, and, instead of remaining 
constantly high through the course of the inflammatory process 
in the skin, goes through marked intermissions or remissions, which 
frequently occur and are followed by rises in temperature as high 
as that which occurred with the first onset. The fever ends in 
some cases by crisis and in others by lysis, the latter mode of ending 
usual] y taking place in those cases which have had a very severe 
attack prolonged in character, or which have been in an asthenic 
state prior to the disease. The diagnosis of erysipelas is easily 
made by the brawny, swollen, and red skin, with the peculiar line 
of demarcation at the edge of the swelling. (See chapter on the 
Skin.) 

A fever which rises sharply from normal to 103 ° or 104 , being 
preceded by a chill and followed in a very few hours by a sweat, 
the whole term of acute illness, if we exclude general physical 
discomfort, lasting but eight to twelve hours, is in the majority 
of cases that of intermittent malarial fever. The peculiarities of 



4-04 



CHILLS, FEVERS, AND SUBNORMAL TEMPERATURES 



intermittent malarial fever, aside from those just named, are that 
the febrile movement begins to decline before the stage of sweating 
begins, and in some cases it begins to rise before the sensation of 
chilliness of the first stage leaves the patient (Fig. 150). 



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Fig. 150. — Showing daily paroxysm due to double tertian infection. One 
set of parasites segmented at 8 p.m., and the second set at 4 p.m. Paroxysm 
stopped by quinine on fourth day. 

The fall of temperature is usually less abrupt than the rise, and 
is sometimes delayed by slight temporary rises or arrests in its 
downward course. The febrile movement is repeated at intervals, 
ranging from one to seven days or even at longer intervals than 
this. If the attacks occur daily, they are called quotidian, and 
this is due to infection by two sets of tertian parasites which 



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Fig. 151. — Showing paroxysms of tertian fever, the segmentation of the 
organisms occurring at about twelve o'clock every other day. 



undergo segmentation on alternate days, or it may be due to 
infection with three sets of quartan parasites. If the attacks 
occur every other day, they are called tertian (Fig. 151); if on the 
third day, quartan; if on the fourth, quintan. If two attacks 
come on the same day, it is called double quotidian. 

Another point of importance in connection with malarial attacks 



FEVER 405 

is that they often occur earlier each day by an hour or more. 
Rarely, they are delayed. 

Intermittent malarial fever is to be separated from other inter- 
mitting fevers by a number of facts. First, the presence of the 
malarial organism in the blood at the time of the attack, or evidences 
of its presence at other times. Second, by the history of exposure 
to malarial influences. Third, by the marked effect for good on 
malarial fever produced by the proper administration of quinine. 

Care must always be taken that the intermitting fever of the 
various forms of sepsis is not diagnosticated as malarial inter- 
mittent fever. The most common error of this character is the 
making of a diagnosis of irregular malarial intermittent, because 
chills, fever, and sweat appear every evening, when, in reality, 
the real cause is an undiscovered pulmonary or abdominal tubercu- 
losis. Again, acute ulcerative endocarditis (see below) and purulent 
phlebitis may cause similar symptoms, as may also hepatic abscess, 
impaction of gall-stones, with suppurative cholangitis, causing the 
so-called Charcot's fever (see below). The absence of a history 
of malarial exposure, the possible presence of a cough, and the 
discovery of a tuberculous lesion in the chest or abdomen by care- 
ful physical examination will aid in deciding that the fever is 
tuberculous and not malarial in origin. (See chapters on the 
Thorax and on the Abdomen.) 

The temperature curve of ulcerative endocarditis may exactly 
resemble intermittent malarial fever; but in many instances the 
presence of an external wound, an acute infection in some part of 
the body, or the presence of the puerperium will reveal the source 
of an infection. (See Fig. 152.) In the typhoid type of ulcerative 
endocarditis the profound asthenia and general prostration will 
separate the disease even if the temperature chart be useless. In 
this form the febrile movement is rarely typically intermittent. 
The crucial test of the differential diagnosis lies in an examination 
of the heart, in which a murmur may be heard in some but not in 
all cases, unless there has already been some grave valvular mis- 
chief. The cardiac feebleness and asthenia, on the one hand, and 
the result of the blood examination, on the other, aid the diagnosis. 
The duration of the case is not of much value in making a diagnosis, 
for cases of ulcerative endocarditis have lasted from two days to 
more than a year. Rarely, it lasts more than six weeks. Death 
usually occurs in ulcerative endocarditis, unless there has been 
previously present chronic endocarditis, in which case recovery 
may rarely occur. 

The discovery of a phlebitis may point to this cause for inter- 
mittent fever. 

The fever of catarrhal or suppurative cholangitis or cholecystitis 
often closely resembles intermittent fever, but the presence of 



406 



CHILLS, FEVERS. AND SUBNORMAL TEMPERATURES 




FEVER 407 

hepatic symptoms, of marked jaundice in the former state, of a 
history of gall-stone colic, and of exceedingly severe rigors, enables 
us to separate them, and swelling and tenderness in the gall-bladder 
will also be present. In obscure cases the malarial organism should 
be searched for, and if the condition be one of cholangitis an 
examination of the blood will probably show leukocytosis. (See 
chapters on Abdomen, Pain, Gall-stone Colic.) 

When fever of an intermittent type has been observed, and 
intermittent malarial fever, tuberculosis, and cholecystitis cannot 
be discovered as a cause, search should be made for tenderness and 
swelling of the liver due to hepatic abscess. Profuse sweats also 
may be found in such cases, as in most instances of septic fever. 
The diagnosis of hepatic abscess will be strengthened if there is a 
history of the patient having suffered from dysentery, as hepatic 
abscess is sometimes caused by amebic dysentery. 

The presence of fever preceded by chills, the temperature rising 
to 104 or even 105 °, followed by excessive sweats, in a person who 
is profoundly cachectic, may be due to pernicious anemia or to 
septic poisoning, as already pointed out; and it should be recollected 
that such a temperature chart is sometimes seen in cases of 
gastric cancer. Similar symptoms as to fever in association with 
enlargement of the lymphatic glands, particularly those of the 
neck, indicate Hodgkin's disease. Tuberculous adenitis, which, 
however, is usually met with in the young, involves the glands 
near the jaw, while in Hodgkin's disease the glands near the 
clavicle are affected. Further, in Hodgkin's disease the swelling 
is usually bilateral, and to be found elsewhere than in the neck. 
Again, in tuberculous disease these glands often suppurate, but 
even if they do so fever usually is absent. The presence of the 
tubercle bacillus in an excised piece of the swelling will decide the 
diagnosis. An intermittent fever may also be seen in suppurative 
pyelitis, in association with pyuria. This pyelitis may or may not 
be tuberculous. 

Remittent fever rising and falling every few days for two or three 
weeks, rarely rising above 103 ° to 104 , and even falling to the 
normal line, associated with enlargement of the spleen and liver, 
yellowing of the skin, or jaundice, bilious vomiting, and a history 
of exposure to malarial infection, is characteristic of remittent 
malarial fever, a form more chronic and very much more grave 
than the intermittent form just described, because it responds 
less readily to treatment; and, secondly, because it is accompanied 
by more marked changes in the viscera. It depends upon infection 
with the estivo-autumnal form of the malarial parasite. The 
conditions produced by this parasite are collectively grouped 
under the names remittent, continued, bilious remittent, and 
typhomalarial fever, or malarial fever of a typhoid type. In some 



408 CHILLS, FEVERS, AND SUBNORMAL TEMPERATURES 

cases the temperature and other symptoms will so closely resemble 
those of typhoid fever that nothing short of an examination of the 
blood can decide the diagnosis. (See Differential Table, page 398.) 

Care should be taken to recollect the fact that when typhoid 
fever develops in a young child the temperature may be so markedly 
remittent that an erroneous diagnosis of malarial infection may be 
made. In other words, " infantile remittent fever" is really typhoid 
fever in many instances. 

A febrile process somewhat closely resembling remittent malarial 
fever, yet so rare, comparatively, as never to be confused with it, is 
Weil's disease. In this condition the fever runs a remitting course, 
is associated with jaundice and swelling of the liver and spleen, and 
the stools may be clay-colored. There is one important point of 
difference between malarial remittent fever and Weil's disease, 
namely, that in the latter gastro-intestinal symptoms are nearly 
always wanting or are mild, whereas in the former they are apt to 
be marked. Usually the fever of Weil's disease ceases by the end of 
two weeks or earlier. It is probably an infectious jaundice. 

In dengue, a disease seen most commonly in epidemics in certain 
parts of the Southern United States, the patient, after suffering 
from violent aching pains in the body and limbs, swelling of the 
joints, and the development of a variable rash on the chest, develops 
an active fever, which lasts with the pain until the fifth day, 
when both the pain and fever decrease or cease, and then often 
return with equal force. These facts, combined with the fact that 
it is an epidemic disease, separate it from malarial fever. Dengue 
and influenza, of an epidemic type, closely resemble one another, 
but in dengue there is rarely marked involvement of the respiratory 
tract as there is in influenza; there is an eruption which is not seen 
in influenza, and it is not followed or accentuated by such grave 
complications as we see in the more severe cases of influenza. 
Dengue is a disease of the South and influenza one of the North. 

The fever of yellow fever is rarely over 103 or 104 , and is one 
of the milder symptoms of the disease; but it possesses this peculiar- 
ity, namely, that after a lapse of from twelve hours to several days 
there is a marked remission of the fever and all the other symptoms 
and from this time on the patient may get well, or after a few 
hours this calm stage is followed by the true violent symptoms of 
the disease, such as black vomit, tarry stools, jaundice, and hemor- 
rhages from the mucous membranes. Generally the full course of 
the disease to convalescence or death is run in about one week. 

There are only two other diseases which can be readily confused 
with yellow fever, namely, dengue and bilious remittent fever. 

Dengue has been confused with yellow fever many times, and 
even the most experienced physicians have had great difficulty in 
separating them when the yellow fever has been mild. The most 



FEVER 



409 



important points in their differentiation are the facts that in 
dengue there is usually a second onset of fever several days after 
the first onset, whereas this does not occur in yellow fever. Again, 
the eruption on the skin is not seen in yellow fever, and a rapid 
pulse is present in dengue, whereas in yellow fever the pulse is 
usually not very rapid. On the other hand, in yellow fever we 
usually meet with jaundice, albuminuria or suppressed urine, and 
a hemorrhagic tendency of a marked degree, all of which are absent 
in dengue. Further, death from dengue is very rare. 

A case of bilious remittent fever occurring during an epidemic of 
yellow fever is almost certain to be incorrectly diagnosticated. In 
the absence of an epidemic, however, the probabilities of the case 
being bilious remittent fever are very great, and the presence of 
bilious vomiting rather than that of blood, the characteristic 
temperature chart, and, above all, the presence of a history of 
malarial exposure and of the signs of malarial infection in the 
blood, with the partial control of the symptoms by quinine in 
certain stages of remittent fever, point to the diagnosis of malarial 
disease rather than to yellow fever. 

Stubhert gives the following differential tables of these fevers: 

Yellow Fever. 



Headache bilateral-frontal, and post-orbi- 
tal. 

Temperature and pulse divergent ; temper- 
ature rarely higher than 104° F. 

Albumin present in large quantities early 
in the disease. 

Quinine has no effect on the progress of the 
disease. 

Stage of remission on third or fourth day. 

Attacks new arrivals. 

Always history of exposure to infection. 
Black vomit appears on third or fourth day. 
Hematuria very rarely present. 
Liver unchanged. 

Yellow Fever. 

Cephalalgia and nephralgia are character- 
istic and constant. 

Pulse and temperature divergent. 

The slowing of the pulse begins early in the 
disease. 

Congestion of face early in the disease. No 
edema. 

Albuminuria. 

Icterus. 

Black vomit. 

No eruption. 



Pernicious Malaria. 
generally unilateral-frontal, and 



Headach 
temporal. 

Temperature and pulse correlative 
perature generally 105° to 107° F. 

Albumin rarely present. 



tem- 



Quinine has a specific effect if given hypo- 
dermically and early. 

Remission not present. 

Generally history of chronic malarial in- 
fection. 

No history of exposure to infection. 

Black vomit appearswitbin thirty-six hours. 

Hematuria a marked symptom. 

Liver enlarged and tender. 

Dengue Fever. 

Pain most severe in joints and muscles, and 
is paroxysmal. 

Pulse and temperature correlative. 

The slowing of the pulse occurs late in the 
disease. 

Bash on face, folloAved quickly by edema. 

Albuminuria absent. 
Icterus absent. 
Black vomit absent. 

Polymorphous eruption, followed by des- 
quamation. 



In spotted fever, or cerebrospinal meningitis, the fever itself is 
one of the least important symptoms, for, aside from the fact that 
it is apt to be irregular and intermitting, it is rarely very high, as 



4IO CHILLS, FEVERS, AND SUBNORMAL TEMPERATURES 

compared with the violent cerebrospinal symptoms, the rigidity of 
the back of the neck, Kernig's sign, the headache, convulsions, 
and vomiting. The presence of these symptoms in an epidemic 
does more to confirm a diagnosis than the febrile movement. In 
some cases of spotted fever, however, of a very grave type, the 
fever becomes a hyperpyrexia, but in cases tending toward recovery 
the temperature usually begins to fall by lysis before any modera- 
tion in the other symptoms is manifested. 

When cerebrospinal meningitis is suspected the physician should 
determine the true character of the affection without delay by 
lumbar puncture. A strong hollow needle supported by a 
trocar is introduced between the second and third, or third and 
fourth lumbar vertebrae and by this means some of the cere- 
brospinal fluid is obtained, which should be received in a sterile 
test-tube, and examined microscopically for the characteristic 
diplococci of spotted fever, and for other microorganisms. ' The 
needle should be inserted 4 cm. (ij inches) in children, and 6 to 8 
cm. (2 to 4 inches) in adults, to reach the fluid in the canal. 
It is not a dangerous operation. Pfaundler, on the other hand, 
recommends that the puncture be made in the lumbosacral space, 
and that it should be performed while the patient is in the sitting 
position. (For area for puncture see the figures on the spinal 
column in the chapter on the Feet and Legs.) In normal persons 
the fluid flows from the needle drop by drop; when the pressure 
is high it spurts. 

He believes that very high pressure of the fluid in the spinal 
membranes is present in tuberculous meningitis, and that this 
high pressure is so rare in other conditions that its presence is of 
diagnostic value. It is found, however, when the patient is suffer- 
ing from purulent meningitis, from spinal tumor, and in some 
cases of functional neurosis. On the other hand, normal pressure 
excludes the presence of meningeal or cerebral affections. If the 
fluid which is obtained contains disintegrated blood, the patient 
is probably suffering from pachymeningitis or injury. If, on the 
other hand, the blood is fresh in its appearance, its presence is 
probably due to the puncture. 

A very important point in this connection, insisted upon by 
Pfaundler, is that if the fluid is clear, every inflammatory affection 
of the meninges, except tuberculosis, may be excluded from the 
diagnosis. In tuberculosis it is often cloudy, and in the later 
stages of the disease nearly always so. If the fluid is purulent, it 
indicates the presence of purulent or epidemic meningitis. A clear 
fluid is found in health, in serous meningitis, hydrocephalus, and 
functional neuroses, and it is generally clear in cases of tumor, 
uremia, and sepsis. The albumin present varies from 0.02 to 
0.04 per cent., and if it is in excess of 0.05, it is probable that the 



FEVER 41 1 

disease is an inflammation or tumor; if it is present in still larger 
amounts, it is probably tubercular meningitis. If, again, on 
analysis of the fluid the normal sugar which it contains should 
disappear, there is probably an inflammatory process present, 
and therefore if sugar is present an inflammation can be to a 
certain extent excluded. 

Even in the presence of an epidemic of spotted fever it should 
never be forgotten that middle-ear disease often causes marked 
meningeal symptoms, and that croupous pneumonia often pro- 
duces a similar train of manifestations, probably by infection with 
its particular microorganism. The possibility of tuberculous 
infection producing such symptoms should cause the physician 
to examine the patient carefully for signs of tuberculous disease 
in other parts of the body from which infection might arise, as, 
for example, the lungs. 

The fever due to septicemia may produce a temperature chart 
which closely resembles that of enteric fever, but septic fever 
generally possesses one characteristic which, in the face of other 
symptoms suggesting sepsis, is of great importance, namely, the 
extraordinary rises from normal to 105 ° or 106 , and from that 
point even to a subnormal degree within a very few hours, so that 
the lines on the chart pass up and down in long sweeps. These 
sweeps are even more sharp and sudden than in an intermittent 
malarial fever, and their cause is determined by the discovery of 
some septic process in some part of the body. The presence of 
such a chart, in association with dull or violent headache, delirium, 
vertigo, and vomiting independent of taking food, would point 
to cerebral abscess, particularly if a history of injury could be 
obtained. 

A somewhat similar chart to this may occur in connection with 
cases of active pulmonary tuberculosis, when the lesions are well 
developed and septic absorption is active; but usually in the hectic 
fever of phthisis we have an approximately normal morning 
temperature, with a rise from 2 to 3 , or even more, toward 
night (Fig. 153). 

This symptom of fever in any form occurring in a person with 
suspiciously "weak lungs" should cause the physician to be confi- 
dent that he has overlooked some focus which another careful 
examination may discover, and it possesses another important 
diagnostic significance, namely, that the more active the febrile 
movement in phthisis pulmonalis the more active the disease 
process, and the less active the fever the less active the process. 
Fever may, however, be almost entirely absent in some tuberculous 
cases with extensive disease of the lungs. 

The febrile movement of acute miliary tuberculosis has nothing- 
characteristic about it, except that in some cases it may closely 



412 



CHILLS, FEVERS, AND SUBNORMAL TEMPERATURES 



resemble that of typhoid fever, and if the physician does not 
carefully examine the case an erroneous diagnosis may be reached. 
If, however, the disease involves the meninges of the brain, a 
hyperpyrexia may be developed, and death speedily occurs in 
such cases, either in the fever or in a sudden collapse. The peculiar 
dyspnea, the cyanosis, the profuse sweats, and the diffuse pulmon- 
ary signs render a diagnosis of acute miliary tuberculosis possible 
in some cases. 




Fig. 153. — Chart of a case of hectic fever, pulmonary tuberculosis, showing 
rising and falling of the temperature morning and night. 

When fever is associated with marked catarrhal symptoms, 
chiefly of the bronchial tubes and upper respiratory tract, with 
sneezing, lassitude, pains in the back and limbs, and excessive 
cough, the fever rising as high as 104 or 105 in severe cases, and 
then falling almost to normal, we may have before us influenza 
or catarrhal fever either of the sporadic or epidemic form. In 
this condition there may be in severe cases great prostration and 
cardiac failure or vomiting and diarrhea. The febrile movement 
is of the most irregular type, even when some grave complication, 
such as severe bronchitis or pneumonia, comes on, although croup- 
ous pneumonia rarely occurs as a complication of "la grippe." 

The respiratory symptoms just described are also seen frequently 
in association with moderate fever, in "hay fever " that condition 
seen in susceptible persons during the haying season or late in the 
summer. 

The fever of acute pneumonia of the croupous type runs a very 
typical course in uncomplicated cases. Following a more or less 
severe chill, the fever quickly mounts to the high point of 103 ° or 
104 , or even more than this (Fig. 154). For the next few days, if 
not modified by the antipyretics and the use of cold, the fever 
remains high; but there may be temporary remissions which look 
as if crisis was about to be established, when in reality they are 
followed at once by a return of the fever (pseudocrisis) . Finally, 



FEVER 



413 



in the majority of cases of croupous pneumonia the temperature 
suddenly falls by crisis on the seventh to ninth day (Fig. 155), 
and convalescence is established, although the sudden fall of 
fever may be associated with dangerous collapse. Sometimes 
convalescence is broken by brief and slight febrile movements. 
If the case has been prolonged, or if it is of the typhoid type, the 
fever may end by lysis. 



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It is to be remembered that the fever of catarrhal pneumonia is 
rarely as high as in the croupous form, usually 101 to 103 °, and 
ends by lysis, not crisis. (See chapter on the Thorax.) 

The fever of acute bronchitis possesses no peculiarities over that 
of other acute inflammations. 



414 CHILLS, FEVERS, AND SUBNORMAL TEMPERATURES 

It is not proper to leave the subject of fever due to the various 
infectious diseases without calling attention to that due to syphilis 
in the secondary period of its course. With the onset of the roseola 
or other skin lesion a fever, more or less marked, is nearly always 
present and is often preceded by chilly sensations and general 
malaise. This febrile movement may then follow one of three 
courses: it may never rise above ioi°, and proceed as does a 
simple fever, with slight morning remissions and evening exacerba- 
tions; or it may be as remittent as is a malarial remittent fever; or, 
again, it may resemble a malarial intermittent, rising to a high 
point and then falling almost to the normal. Phillips, of London, 
has reported a case of syphilitic fever in which this febrile move- 
ment lasted for weeks, and, after being treated by quinine as a 
supposed tertian ague, without effect, ended at once under anti- 
syphilitic medication. (See chapter on the Skin, Eruptions.) 

The fever of ordinary cases of acute articular rheumatism is 
usually moderate, rarely exceeds 103 °, and possesses no typical 
characteristics ; but in very severe forms of the disease with cerebral 
manifestations, a rheumatic hyperpyrexia may be developed, 
when, with delirium, convulsions, and cyanosis, the fever rises to 
106 and even to 108 , after which death often ensues. The 
history of previous attacks of articular rheumatism, the hot, 
swollen joint or joints (usually the large ones), and the successive 
invasion of other joints as the ones first affected get well, point 
to the correct diagnosis. It must not be forgotten, however, that 
gonorrheal and other forms of septic arthritis occur with febrile 
movement. Pyemia, osteomyelitis, and purpura also may produce 
a fever with swelling of the joints. (See chapter 1 on the Legs 
and Feet.) 

When a person, previously afebrile, during hot weather or when 
exposed to artificial heat in excess, is attacked by unconsciousness, 
convulsions, and very high fever, he is probably suffering from 
thermic fever or heat-stroke. Theoretically similar symptoms 
might be caused by a lesion due to embolism or hemorrhage in 
the neighborhood of the pons Varolii, but this is very rare. (See 
chapter on Hemiplegia and the Face and Head.) The fever in 
sunstroke may rise as high as no° or 112 or even more; the 
skin is hot and dry, or more rarely cold and moist with sweat; 
but, even if this is the case, the rectal temperature will be found 
hyperpyretic. 

A great rise of temperature (no° to 112 °) often occurs after 
injuries to the cervical region of the spinal cord. 

The rapid development of fever, pain in the back and limbs, 
and particularly in the nerve trunks, the temperature soon reaching 
103 ° or 104 , may be due to an attack of acute multiple neuritis, 
and the history that the illness has followed exposure to cold and 



SUBNORMAL TEMPERATURE 415 

wet may, on the one hand, make the physician believe that his 
case is suffering from rheumatism or influenza, or on the other, 
in the absence of such a history, from the early stages of one of 
the infectious diseases. The early appearance of tingling, numb- 
ness, loss of power, and wasting of the muscles soon decides the 
diagnosis in favor of neuritis. The nervous disease which most 
closely resembles acute febrile neuritis is Landry's paralysis, 
and a differential diagnosis may be difficult; but in neuritis there 
are loss of sensation, muscular wasting, signs of degeneration, 
and fever, whereas in Landry's paralysis all these are wanting, 
excepting the sensory symptoms, which in both diseases may be 
similar. The predominant symptoms of Landry's paralysis are 
rapid paralysis and loss of reflexes. (See chapter on the Legs and 
Feet.) 

The prognosis of the severe form of febrile neuritis is grave, as 
death may ensue from respiratory paralysis. 



SUBNORMAL TEMPERATURE. 

Subnormal temperature of the body is seen as the result of 
any profound nervous shock, as after an accident or surgical 
operation, or prolonged anesthetization. It occurs, too, at the 
ending of the fever of croupous pneumonia and other febrile 
movements ending by crisis. It is also seen in severe cholera 
morbus and cholera Asiatica and sometimes in cholera infantum, 
and often is present either in the early part of the cold stage of 
intermittent malarial attacks or more commonly after the fever 
of the attack has fallen. A subnormal temperature of a dangerous 
degree is met with in the algid type of pernicious malarial infec- 
tion, and can only be satisfactorily differentiated from other con- 
ditions by a blood examination. Subnormal temperatures are 
also seen in some cases of confusional insanity and of tuberculous 
meningitis and hysteria. 

An important variety of subnormal temperature is that seen in 
the form of heat-stroke called heat exhaustion, when, in place of 
fever, a condition of collapse is induced. 

Severe injury to the dorsal region of the spinal cord often pro- 
duces a great fall of temperature. 

A temperature below 92.3 is nearly always fatal in its prog- 
nosis, but subnormal temperatures above this degree are not 
necessarily followed by death. A temperature of 95 ° is spoken of 
as one of moderate collapse. 



CHAPTER XV. 
HEADACHE AND VERTIGO. 

The causes of headache — Digestive headache — Headaches due to the eyes — 
Headaches due to cerebral growths and abscess — Headaches due to syph- 
ilis — Headaches complicating acute diseases. 

HEADACHE. 

Headache is, of course, always a symptom and never a disease, 
and it arises from such widely different causes that it is impossible 
in this book to discuss all of them. Only the more common con- 
ditions resulting in its development can be considered, more 
particularly in relation to its diagnostic significance in serious 
pathological states. The most common cause of headache is 
probably disorder of function in the digestive apparatus, the 
next most common cause is eye-strain in its various forms, and 
the third is nervous exhaustion or neurasthenia with or without 
associated anemia. These may all be considered as perversions 
of function causing headache — that is, the pain in the head may 
be termed a functional headache. Less frequent, but far more 
important from a diagnostic standpoint, is headache seen in 
persons suffering from renal disease, brain tumor, and meningitis 
in its various forms. The remaining causes of headache are numer- 
ous, and some of them will be considered later; but the most im- 
portant of the first class are so called bilious headaches, the head- 
aches of the gouty or the rheumatic, and of the second class those 
of middle-ear disease, meningitis, cranial periostitis and acute 
inflammation of the eye or in the jaw. 

Headaches depending upon disturbances of the digestive system 
are nearly always accompanied by evidences of such disorder, 
consisting in gastric or intestinal distress, belching, hiccoughing 
or vomiting, and often constipation. Often there is a distinct 
history of the ingestion of indigestible food or digestion-disturbing 
drink, but in other cases exposure to cold so congests the abdominal 
viscera that catarrh of the stomach and bowels is induced, and 
with it congestion of the liver followed by jaundice. The head- 
ache of disturbed digestion is nearly always frontal, and in many 
cases congestive to such an extent that the face may be flushed, 
or at least the intracranial circulation is so disturbed that the 
patient is unable to lower the head, because such a posture increases 



HEADACHE 417 

the pain. Such cases are relieved by hot foot baths which relieve 
the congestion of the head; nearly always by the act of vomiting, 
which should be induced, if need be, by an emetic or by putting 
the finger into the back of the throat. Vomiting makes such 
headaches very much worse for a time, owing to the congestion 
of the head following the efforts at vomiting, and this is an impor- 
tant point in diagnosis, for in uremia due to renal disease and 
in some other states the vomiting is often so easily performed 
that no straining accompanies it. 

That disturbances of the digestive tube are capable of altering 
the intracranial circulation is proved by numerous facts. Thus 
Brunton quotes the experiments of Ludwig and Dogie], who 
showed that moving the intestines by the finger introduced through 
an abdominal incision caused a great increase in the flow of blood 
through the carotid arteries. 

Headache due to disorder of the digestion rarely ensues immedi- 
ately after food is taken, since some time must elapse before the 
ingested material becomes changed into an irritating or toxic mass 
by fermentation or putrefactive processes. As a consequence, 
several hours or even a day may pass without any discomfort in 
the head, after which time the full force of the headache develops. 
The headaches of indigestion are, however, characterized by two 
important facts, viz., that they are not constant, and, second, 
that they are often relieved or prevented by the use of a purgative, 
even if constipation has not been present. Such headaches are 
very apt to be pulsating and accompanied by great nausea. Some- 
times such a headache takes a form called migraine, or henii- 
crania, a condition in which the pain is chiefly, if not entirely, 
unilateral, and there may be associated with the pain early, and 
more or less persistent, hemianopsia. It is to be remembered, 
however, that in some cases of hemicrania of nervous origin the 
sickness at the stomach seems to be secondary to the severe pain 
in the head. 

Headaches resulting from digestive disturbance do not always 
depend entirely upon irritation of the stomach and bowel with 
reflex disturbance of the circulation and sensory nerves of the 
head, but upon the absorption of poisonous substances formed in 
the digestive tube. These poisons are usually formed only to be 
destroyed by the liver, or are developed in too small quantities 
to have any effect; but no sooner do congestion of the liver and 
deficient biliary secretion ensue than they are formed in large 
amounts, and enter the general blood stream, owing to the absence 
of antiseptic bile and the coincident or consequent constipation. 
As a result, we see very violent headache in jaundice due to 
catarrhal changes, particularly if the kidneys are not active in 
the elimination of toxic substances. 
27 



4l8 HEADACHE AXD VERTIGO 

In other cases in which no jaundice is present violent headaches, 
which utterly incapacitate the patient, come on from auto-intoxica- 
tion. Thus, a man apparently perfectly well goes to bed on a 
certain night and wakes in the morning feeling a little more drowsy 
than usual. On rising he may feel a little stupid, and perhaps be 
slightly vertiginous, but is able to eat his breakfast as heartily as 
usual. In the course of a few hours the mental heaviness becomes 
more marked and a pain in the brow develops, which gradually 
gets worse and worse until it is unbearable. The ordinary remedies 
for neuralgic headache are futile, and he finds no relief until by 
the use of a purgative he removes the source of his intoxication, 
and his kidneys have time to eliminate the toxins already absorbed. 
Sometimes vomiting comes to his relief, and the emptying of the 
stomach so stimulates his liver and intestines 'by the efforts of 
vomiting that the process of auto-intoxication ceases. Some of 
the intestinal poisons have been isolated by Brieger, Harnack, and 
others, and have a physiological action like many well-known 
drugs. Thus, one produces effects like those of digitalis, another 
like those of belladonna, and a third like those of aconite. Pulsat- 
ing pain and a slow, full pulse may indicate the absorption of the 
digitalis-like toxin; a flushed face and hot, dry skin, the belladonna- 
like toxin; and pallor, faintness, and a feeble pulse, if no nausea 
is present, the presence of the aconite-like toxin. Persons suffering 
from headache of this type are nearly always much freer from 
discomfort in the head after such an attack than they have been 
for some time before. 

Brunton has also pointed out that digestive headaches are often 
associated with an objective and subjective sensation of increased 
intra-ocular tension and tenderness on the upper surface of the 
eyeball, and the author has frequently confirmed this observa- 
tion. 

The headache of eye-strain is usually due to abnormalities in the 
ocular muscles. Most commonly, according to Noyes, the externi 
(abductors) are the muscles which are the seat of the difficulty, 
but this opinion is not generally shared by other ophthalmologists, 
who assert that the interni are most commonly at fault. Such 
headaches may be felt in any part of the head, but are most 
commonly said to be in the occipital region. If, in association 
with such headache, immediately after or long after reading there 
is blurred vision, pain in the muscles of the eye on suddenly moving 
the eyeball, a tendency to congestion of the lids, or hyperemia in 
the conjunctiva over the insertion of the muscle, the diagnosis of 
headache from eye-strain is practically certain. (See chapter on 
the Eye.) Violent pain in the head may also be due to irritable 
retina and to astigmatism and spasm of the ciliary muscle. Acute 
inflammatory processes in any part of the eye may produce severe 



HEADACHE 419 

headache, particularly iritis, the pain of which is very apt to be 
worse at night. 

Violent headache is often produced by acute or chronic glaucoma, 
and is usually felt about the eyes or orbit. Often it is of a unilateral 
character, and the sharp, shooting pain causes a false diagnosis of 
neuralgia to be made, or in some cases the patient is thought to be 
suffering from migraine, because in addition to unilateral pain there 
are often nausea, vomiting, and pallor of the face. The examina- 
tion of the eye will show glaucoma to be present. Quite similar 
symptoms may appear as the result of a foreign body lodged in the 
cornea. 

The headache associated with nervous exhaustion or neurasthenia 
may be superficial or deep; that is to say, neuralgic or apparently 
within the skull. It is often associated with some dizziness and 
vertigo, and is nearly always occipital in character, more rarely 
appearing over the brows. In addition to the pain, which is 
generally not very severe, there is often a sense of constriction 
about the head. Such a headache persists as long as a person 
who is overworked persists in fatiguing himself, and rapidly 
disappears when rest is taken. More rarely the pain in the head 
in neurasthenia is that of migraine, and is complicated by hemi- 
anopsia and hemicrania, often by a dilated pupi) on the affected 
side, and flushing and pallor of one side of the face. 

Headaches due to rheumatism are often quite severe, and are 
associated with much tenderness of the scalp or muscles covering 
the skull. Similar headaches, but more dull in character, are 
also seen in persons suffering from phosphaturia, and are relieved 
by benzoate of ammonium. 

A headache is a symptom very commonly seen in persons who 
are subject to the chloral habit, and it may be general or limited 
to the forehead. It is commonly associated with vertigo, flushing 
of the face, and intense heaviness and drownsiness. 

Headache of a violent, bursting character may be produced by 
full doses of nitroglycerin, the salicylates, and quinine, and by the 
use of large quantities of certain kinds of tobacco. 

Leaving the headaches due to functional disturbances not 
associated with organic change, we pass to those due to organic 
disease. Those due to renal disease are of two classes. They are 
an evidence of uremia, or they are congestive and due to the high 
arterial tension so often seen as the result of chronic contracted 
kidney with its associated conditions of cardiac hypertrophy and 
arteriosclerosis. Uremic headache, as pointed out in the chapter 
on Vomiting, is often associated with nausea or vomiting of a 
persistent type, and sometimes with diarrhea, for purging is an 
effort at elimination. The pain is not of the shooting, darting, 
or neuralgic type, but dull, even if severe, and is often associated 



420 HEADACHE AND VERTIGO 

with a sensation of fulness in the head. Sometimes the tendency 
to drowsiness is very marked, and, even if the patient does not 
sleep, he may seem on the verge of sleep all the time. Not rarely 
these cases instead of becoming comatose become wildly delirious. 

These uremic headaches may occur in any form of renal disease, 
acute or chronic, which results in uremia; but, if the cause be chronic 
contracted kidney, there will be usually a high arterial pressure, 
and often a strongly beating heart with an accentuated second 
sound. This form with high arterial pressure will often be relieved 
by full doses of nitroglycerin, which not only relieves the tension, 
but also produces an increased renal activity. The urinary examin- 
ation is of the utmost importance, and no surely correct diagnosis 
can be made in any case of suspected kidney trouble until this 
secretion has been examined and found abnormal. 

Curschmann has shown that in threatened uraemia a Babinski 
reflex, that is, extension of the toes, develops on irritating the sole 
of the foot. 

While headache is far less common as a symptom of diabetes than 
of nephritis, it occurs in the former disease either as a dull pain 
with lassitude and depression of spirits or as a violent neuralgia, 
due to the starved state of the tissues. 

Headache which is constant, although it usually varies in degree, 
may be due to brain tumor, and is one of the most important 
symptoms to be noted in the diagnosis of a case in which such a 
lesion is suspected. The pain is often worse at night, and is usually 
more severe in persons suffering from tumor of the cerebellum 
than in cases in which the growth is in the cerebrum, probably 
because cerebellar growths often cause effusion which produces 
pressure inside the skull. A tumor of the cerebral cortex, as a 
rule, produces more pain than one in the white matter beneath. 
Meningeal growths are also apt to produce severe headache, but 
bony tumors of the skull often press upon the brain to an extra- 
ordinary degree without causing any symptoms. 

Headaches due to brain tumor often have exacerbations with a 
regularity suggesting malarial disease, and, conversely, care should 
be taken not to mistake malarial headache for brain tumor. 

After constant headache, the most valuable confirmatory 
evidence of brain tumor is papillitis of the optic nerve, which is 
present in about 80 per cent, of the cases. There may also be 
vomiting and convulsions if the growth be in the motor cortex. 
Local paralysis, indicating the position of the growth, may be 
entirely absent, or it may exist and yet utterly mislead the phy- 
sician as to the focal area which is diseased, since cases are on 
record in which, for example, a hemiplegia has existed, and at 
the postmortem examination the growth has been found in the 
frontal lobes. 



HEADACHE 42 1 

Tumors of the base of the brain cause focal symptoms most 
commonly, and in addition to unilateral choked disk we find in 
many such cases ptosis from paralysis of the oculomotor nerve, 
disturbances in the functions of the trifacial nerve in its sensory 
filaments, so that painful tic (see chapter on the Face and Head) 
or anesthesia of the face may be present, and complete unilateral 
facial palsy may occur. If the hypoglossal nerve is affected by 
the pressure, the tongue is protruded to one side, it develops hemi- 
atrophy, and disorders of speech result. Hirt points out that 
a tumor in the anterior fossa is apt to produce paralysis of the 
olfactory and oculomotor nerves and the upper branch of the 
trifacial. 

A tumor in the pituitary body causes pressure on the chiasm 
with resulting amaurosis, ptosis from oculomotor palsy, internal 
squint from paralysis of the abducens (sixth), and anesthesia 
of the skin and muscles of the eyebrow, forehead, nose, and eye, 
from involvement of the first division of the trifacial. Asso- 
ciated with these symptoms there may be disturbances of nutrition, 
particularly as to the genitals and the lung structures. A tumor 
of the middle fossa above the dura causes oculomotor palsy 
(ptosis), patheticus paralysis (downward deviation of eyeball from 
paralysis of the superior oblique), and amaurosis from pressure 
on the chiasm. On the other hand, if it is below the dura, the 
oculomotor, the pathetic, the abducens, and the fifth nerve are 
paralyzed. 

When tumors occur in the posterior fossa they cause paralysis 
of the trifacial, facial, auditory, glossopharyngeal, vagus, spinal 
accessory, and abducens, or, in other words, cause anesthesia of 
the upper part of the face, facial paralysis, deafness, loss of taste, 
irregular cardiac action loss of power in the sternomastoid and 
trapezius muscles, and internal squint. Tumors of the lenticular 
and caudate nucleus, the interior portion of the thalamus, the corpus 
callosum, the fornix, choroid plexus, and of any part of the cere- 
bellum except the vermiform process, may be present without 
any localizing signs. 

Still more localizing symptoms are early paralysis of the oculo- 
motor nerve from a lesion in the crus, hemianopsia in tumor of 
the occipital lobe, and tonic convulsions with preservation of 
consciousness and a staggering gait in tumor of the vermis of the 
cerebellum. 

Should amaurosis be present, very valuable data as to the 
position of the growth are to be had from a study of the functions 
of the eye. If the pupils react properly to light, this shows that 
the optic nerves and tracts are intact, or, in other words, that the 
ocular reflex arc is perfect, and that the lesion must be in the ocular 
centres farther back. On the other hand, if the reflex is absent 



422 HEADACHE AXD VERTIGO 

the growth probably presses on the nerve or tract. (See chapter 
on the Eye.) 

The failure of a pupillary reaction may, however, depend upon 
amaurosis from lateral hemianopsia, in which case we examine the 
patient for what is known as " Wernicke's sign of hemiopic pupil- 
lary inaction." This is done by throwing the light by the oph- 
thalmoscope so that it falls upon the blind half of the retina. If 
the pupil does not react, we have in all probability a lesion of the 
optic tract of that side; whereas, if the pupil does react, we have 
evidence that the tract is intact, and there must be a bilateral 
lesion of the optic radiations of the occipital lobes, or in the centre 
of vision in the cortex. (See chapter on the Eye.) 

Other general symptoms of brain tumor are slow breathing, 
particularly when the patient sleeps, a slow pulse, and, as the 
growth increases, symptoms of cerebral compression. It ought 
to be remembered that brain tumor may be closely masked by 
the results of chronic nephritis, for in the latter disease we find 
headache, local palsies or spasms, and, more important than all, 
an optic papillitis, which used to be thought pathognomonic of 
brain tumor. Albuminuria may be present in both diseases, but 
tube casts can usually be found in renal disease and not in tumor. 
Both diseases may, however, exist side by side. 

Care should be taken in a case of constant and severe headache 
that it be not thought due to brain tumor until the possibility of 
its being caused by a syphilitic arteritis, syphilitic meningitis, or 
syphilitic gumma, is excluded, for mental depression and crashing 
head pains occur in all of these states. This is the more important 
because arteritis occurs as the most common result of syphilis, 
meningitis is next in frequency, while gumma is the least frequent 
of all the cerebral complications of lues. The differentiation of 
gummatous tumor from cerebral tumor due to other causes may 
be impossible unless there be a history of specific infection or 
manifestations of syphilis in scars or other external signs of 
syphilis. Improvement in the symptoms under the use of iodides 
and mercury would indicate syphilis rather than a growth due 
to other causes. The presence of optic neuritis would indicate 
tumor or meningitis, and would exclude arteritis; and in tumor 
the pain is apt to be localized, while in arteritis and meningitis 
it may be diffuse. The chief symptoms of arteritis are those 
indicating failure of a proper blood supply to the brain, as 
evidenced by giddiness, weakness of groups of muscles, difficulty 
in speech, so that words are dropped out, and, it may be, in addi- 
tion, the presence of symptoms like general paresis. Paralysis, 
when it develops elsewhere than in the ocular muscles, in such 
cases is usually the result of arteritis, since the arteritis results in 
a thrombosis; but when the ocular muscles are affected the lesion 



HEADACHE 



423 



is probably due to meningitis or to nuclear lesions. This develop- 
ment of ocular palsy is a great diagnostic significance. (See chapter 
on Eye and Face and Head.) In meningitis the symptoms are 
irritative, such as spasmodic paralysis and irritative fever. 

The following differential diagnostic table aids in making a 
diagnosis; but it is to be remembered that all these conditions may 
be very obscure : 



Syphilitic Arteritis. 

Headache diffuse, often ab- 
sent; not severe. Not started 
by pressure on cranium. 



Hemiplegia or monoplegia 
frequent. Muscles affected 
are flaccid, and reflexes are ab- 
sent. Paralysis often fleeting 
and limited to a few groups of 
muscles. 

Optic papilla usually normal, 
sometimes syphilitic retinitis 
is present. 

Partial epilepsy rare. 

Aphasia is transitory and in- 
termittent. 

Hallucinations rare. 
Pain in limbs rare and fleet- 
ing. 

Intellectual functions feeble. 

No active delirium. 
Ocular symptoms rare. 



Disorders of sensation are 
fleeting. 

Paralysis of cranial nerves 
not common. 



Temperature may be raised. 



Syphilitic Meningitis. 

Headache diffuse and rqrely 
wanting; sometimes localized. 
Started by pressure or by per- 
cussion on head. Very severe. 

Paralysis, if present, associ- 
ated with rigidity and con- 
tracture, involuntary spasms, 
exaggerated reflexes. Paralysis 
more widespread. 

Optic retinitis with marked 
neuro-retinitis and abundant 
exudation along the vessels. 

Partial epilepsy common. 

Aphasia less complete but 
more permanent. 

Hallucinations common. 

Severe pain in limbs of cen- 
tral origin. 

Intellectual functions not 
feeble, but may be drowsy. 

Active delirium often present. 

Bitemporal hemianopsia due 
to compression of the chiasm. 
Homonymous hemianopsia. 

Amaurosis from pressure on 
optic tracts. 

Permanent zones of hyper- 
esthesia, ansesthesia, and par- 
esthesia. 

Paralysis of any cranial 
nerve. 



Temperature quite frequently 
raised. 



Syphilitic Gumma. 
Headache usually localized. 



Distinct focal paralysis com- 
mon. Paralysis associated with 
rigidity and spasm. 



Choked disk often present. 



Hallucinations rare. 



Ocular symptoms of gumma 
involve ocular cranial nerves 
(see text). 



Paralysis of cranial nerves if 
gumma is so placed as to injure 
them. 

Temperature very rarely 
raised. 



So far as the diagnosis of syphilis is concerned, the history of 
infection and the Wassermann reaction, applied to the blood and 
cerebrospinal fluid, will make a decision possible. 

In connection with the above table, it must be remembered that 
should the arteritis result in degenerative changes descending the 
pyramidal tracts, or in thrombosis with degeneration, the flaccid 
paralysis characteristic of arteritis may become spastic. Again, 



424 HEADACHE AND VERTIGO 

should aneurysm arise from the arteritis the pressure upon a 
cranial nerve may produce paralysis, as does meningitis. Then, 
too, the meningeal symptoms may be varied. If the lesion is acute 
and at the base, there will be vertigo, compression of the cranial 
nerves, polyuria, and bulbar phenomena, and finally fatal coma. 
If it be at the convexity, then noisy delirium, convulsions, hallu- 
cinations, and paralysis in the form of hemiplegia or monoplegia 
appear. Death comes in coma. If it is chronic meningitis of the 
base, then we may have slowly developing alternate hemiplegia, 
crossed paralysis of the face and body, anesthesia of one side of 
the face, and paralysis of motion on the opposite side of the body. 
If the convexity be affected then great irritability of intellection, 
sensation, and motion may be present. Paralytic strokes are 
common, but coma is rare. 

Violent headache is the most marked symptom of brain abscess; 
but focal symptoms — that is, localized palsy pointing to the area 
of the abscess — are very often absent, although the localizing 
symptoms which have just been described as due to tumor may, 
of course, be due to abscess if it is so placed as to press on nerve 
tracts or centres. 

The rises of temperature which frequently occur in cerebral 
abscess are also indicative of the presence of pus, while the more 
rapid course of the disease, often only one or two weeks, points to 
abscess rather than tumor. Further than this, choked disk is 
rare in abscess and common in cases of tumor. 

The difficulty of separating the headache of brain tumor from 
that due to brain abscess is very great, for the symptoms with the 
headache are almost if not quite identical in both cases. One of 
the most important of the differential points is the history of an 
injury to the head or of the presence of an infecting focus which 
could have caused cerebral abscess. Another means of aiding 
diagnosis is to examine the blood for leukocytosis. If the white 
cells are excessive, abscess is probably the cause of the illness. 

In some cases of acute cerebral abscess, particularly in children, 
there is a curious tendency to bore the head into the pillow, or, 
if the child is still about the room, the head is rubbed or butted 
into the wall or against the body of the nurse. These symptoms 
are, however, absent in the slow, insidious forms. 

When the physician has made a diagnosis of cerebral abscess 
because of the headache and associated symptoms, he must not be 
misled into a reversal of his diagnosis by marked improvement in 
the patient, who may so far recover as to go back to his occupation, 
for it sometimes happens that a remission or latent period develops 
in the subacute forms of abscess. During this apparent remission, 
however, the temperature is rarely constantly normal, the patient 
is anything but well, and chills may recur. 



HEADACHE 425 

Severe headache well diffused over the skull, coming on rather 
rapidly and associated with fever, stiffness of the back of the neck, 
vomiting, photophobia, delirium, and, finally, stupor and paralysis, 
is probably due to meningitis or to tuberculous meningitis, effusion 
at the base of the brain, or, more rarely, to the onset of a severe attack 
of one of the acute infectious diseases. The differentiation of the 
former from the latter is sometimes difficult, but the rinding of 
some local tuberculous focus, the insidious nature of the onset in 
some cases, the family history, and a set of symptoms pointing 
strongly to involvement of the base of the brain indicate that the 
bacillus tuberculosis is the cause of the disease. Then, too, tuber- 
culous meningitis is rare in persons past middle life. The fact 
that these symptoms are due in some cases to the onset of one of 
the acute exanthemas is established promptly by the appearance 
of a rash. 

If the disease be tuberculous meningitis, the head pains will often 
be paroxysmal in character, so that the patient will at intervals 
of varying length give vent to sharp cries, evidently due to a 
sudden dart of pain. Vomiting may also be present and ocular 
symptoms develop, such as ptosis, strabismus, and unequal pupils, 
which have a sluggish reaction. The febrile movement will be 
irregular, now high, then very low; the temper peevish, if con- 
sciousness is present; and the skin pale and transparent. In the 
severe and rapid cases of tuberculous meningitis marked delirium 
comes on, the patient picks the bedclothes, and there are tender- 
ness and stiffness of the nape of the neck. Pulmonary signs of 
tuberculous disease are often present, and even if absent a focus 
of tuberculous disease can often be found elsewhere. Care 
must be taken that the case is not mistaken for and thought to 
be typhoid fever, which it may closely resemble in its early stages, 
when headache, malaise, languor, and remitting delirium are 
present. 

In children these symptoms of tubercular meningitis may be 
so marked as to lead the physician to the diagnosis of this disease 
almost at once. Usually for some two or three weeks before the 
onset of the severe symptoms the child will have been feverish 
and cross. Vomiting of a more or less obstinate form now comes 
on, and constipation is present. The pulse becomes slow and 
irregular, a mild fever is present, and emaciation may be rapid 
The general nervous state is one of apathy, but finally may be 
disturbed by the sharp hydrocephalic cry. Often the child makes 
chewing or sucking movements. The fact, however, that several 
other conditions produce identical signs in this class of patients 
renders caution necessary. It has just been pointed out that the 
onset of an infectious disease may so result, and it is to be remem- 
bered that inflammation of the middle ear of an acute type with 



426 



HEADACHE AND VERTIGO 



or without brain abscess, may cause every one of the symptoms 
just described. Such cases are often incorrectly diagnosticated 
until a discharge from the ear with great relief to the patient 
clears up all doubt as to the malady. Then, again, in some cases 
of croupous pneumonia all pulmonary symptoms may be masked 
in the violence of the meningeal manifestations, and, finally, it 
is not to be forgotten that in some cases of severe gastro-intestinal 
disorder there may be signs of meningeal inflammation, such as 
coma, squint, convulsions, myosis, Cheyne-Stokes breathing, and 
a depressed fontanelle. 




Fig. 156. — Kernig's sign, showing the strong contraction of the flexors on 
attempting to extend the leg. (After Osier's case.) 

A valuable symptom of tuberculous meningitis is change in the 
optic disk which may be distinctly swollen. Another ocular 
symptom of importance is the presence of tubercles in the choroid. 
The first of these is rarely present in cerebrospinal meningitis, and 
is common in tuberculous meningitis. The second is character- 
istic but is not commonly seen of tuberculous meningitis. Another 
means of diagnosis of tuberculous meningitis is by lumbar puncture. 
A large, hollow needle is inserted at the side of the third or fourth 
lumbar vertebra in a line drawn between the iliac crests across the 
back. If the needle is inserted properly the subarachnoid fluid 
speedily escapes from it. This fluid, if centrifuged, may, in a fair 
percentage of cases of tuberculous meningitis, reveal the presence 
of tubercle bacilli. Another indication that the case is tuberculous 
is the finding in the subarachnoid fluid of an excess of lymphocytes. 
While this excess of lymphocytes is not diagnostic of tuberculous 
meningitis, it is, when taken in connection with the other signs 



HEADACHE 427 

of the disease, of great diagnostic importance, and excludes the 
acute purulent forms of meningitis in which an excess of poly- 
morphonuclear cells are present. 

Koplik believes in the value of percussion of the skull in 
this disease in young children. The child should be upright, 
with the head slightly inclined to one side, and the percussion 
made at the junction of the frontal, parietal, temporal, and great 
wing of the sphenoid bones; in other words, about one and one- 
quarter inches behind the external angular process of the orbit. 
If, in percussing this area, a tympanitic note is developed, fluid 
is present in the latter ventricles of the brain, and tuberculous 
meningitis is probably present. Koplik believes that the per- 
cussion of the skull in the earlier stages of tuberculous meningitis 
is one of the most valuable aids in diagnosis. This sign can be 
developed only in very young children. 

In some cases of typhoid fever meningeal symptoms develop, 
some of these the autopsy fails to show any signs of meningeal 
trouble. In others a true meningitis is found. 

A valuable sign indicative of all types of meningitis is that of 
Kernig. The patient is placed in a sitting posture at the edge of 
the bed, with the feet on the floor. If meningitis be present, it will 
be found that the leg cannot be extended on the thigh, because of 
contractures in the muscles. If the patient is too ill to sit up, then 
he should be placed on his back, the thigh flexed on the trunk and 
the leg on the thigh, and an attempt made to straighten the leg, 
which attempt will fail in a large number of cases if meningitis is 
really present, the hamstring muscles becoming rigid and cord-like. 

Another valuable diagnostic test of meningitis is the development 
of the contralateral reflex. This consists in flexing one leg on the 
thigh, when it will be found that the other leg is also flexed more 
or less completely. Still another test is the one called Brudzinski's 
reflex. The child being in the dorsal decubitus, the hand of the 
physician is placed under the head, which is flexed on the chest. 
As this is done the legs and arms on both sides are drawn up in 
flexion. 

Somnolence or delirium may be present with many of the charac- 
teristic symptoms of meningitis. This condition usually arises in 
connection with chronic exhausting diseases, such as long-continued 
diarrhea and the continued fevers. 

The symptoms of meningitis closely resemble those due to throm- 
bosis of the cerebral sinuses, so closely, indeed, that only the presence 
of the typical signs of such occlusions can determine the diagnosis. 
Thus, if the superior longitudinal sinus is affected by thrombosis, 
there may be epis taxis from distention of the nasal veins, and the 
temporal veins will be swollen, and the nearby tissues edematous 
through their close connections with the sinus through the emissary 



428 



HEADACHE AND VERTIGO 



veins of Santorini, which escape from the skull by way of the 
parietal foramina (Fig. 157). In children there is usually in such 
cases bulging of the fontanelles and heaviness. 

Thrombosis of the cavernous sinus is usually accompanied by 
quite typical symptoms. There is edema of the eyelids and finally 
of the entire side of the face on the side of the affected sinus, but 
this facial symptom may be absent or very fleeting in its duration. 
Sometimes there is exophthalmos, and if the thrombus is septic a 
phlegmonous inflammation of the orbital connective tissue may 
occur. These symptoms are due to the communication between 



Communication through parietal 

foramen rcith externaVveins of skull. 




Ext. jugular vein, 

Int. jugular 
vein 

Fig. 157. — Showing the communications existing between the superior 
longitudinal and lateral sinuses and the external veins, indicated in the figure 
by *. (Leube.) 



the sinus and the ophthalmic veins. Finally, as pointed out in the 
chapters on the Face and Head and on the Eye, paralysis of the 
oculomotor nerve, the ophthalmic branch of the fifth nerve, and 
of the abducens and patheticus may occur, as these nerves pass 
through the cavernous sinus or in its walls. Nearly always throm- 
bosis of the cavernous sinus results from some disease processes 
near by, as in disease of the middle ear and mastoid. Sometimes 
the affection is bilateral. 

If the lateral sinus is affected by thrombosis, there is usually 
marked edema back of the ear, owing to the clot extending to the 



HEADACHE 



429 



small veins of the scalp, which pass through the mastoid and 
posterior condyloid foramina. The external jugular vein on the 
affected side is partly collapsed, particularly on full inspiration 
(Gerhardt's symptom). Rarely, this vein may be unduly distended 
(Fig. 158). Thrombosis of the lateral sinus occurs far more fre- 



Ant. facial vein 




jExt. jugul vein 



Communication with veins 
at back of neck 



Fig. 158. — Showing the communications existing between the lateral and cavern- 
ous sinuses and the external veins, indicated in the figure by *. (Leube.) 



quently than that of the other sinuses. Suppurative otitis is 
its most common cause, and agonizing earache is, therefore a 
symptom often associated with it. 

Not only may cerebral thrombosis present symptoms resembling 
those of meningitis, but in addition those of cerebral abscess. 

Violent headache, with vertigo, staggering, and confusion of 



43° HEADACHE AND VERTIGO 

thought, followed by unconsciousness, may follow meningeal hemor- 
rhage due to disease of the bloodvessels, which are ruptured by 
some strain or by increased blood pressure under the influence of 
stimulants. Hemiplegia or localized spasms may be present. The 
patient may survive several days in severe cases, or may recover if 
the hemorrhage is small; but usually a hemorrhage large enough 
to cause marked symptoms is large enough to cause death. 

The individual affected by meningeal hemorrhage will usually 
have a history of injury, and, with the symptoms just described, 
will suffer from photophobia, extreme sensitiveness to the slightest 
noise, and pain radiating down the neck and trunk, which occurs 
in paroxysms. Localized paralysis is rarely present. 

The presence of severe vertical headache in a middle-aged person 
who is insane and who is a male may indicate pachymeningitis 
interna hemorrhagica (hematoma of the dura); but usually the 
insane patient does not complain, and an antemortem diagnosis 
of this state is not made. 

Headache resulting from heat-stroke or thermic fever is usually 
the result of meningeal congestion or inflammation, and is one of 
the most annoying symptoms of convalescence. It is apt to be 
greatly increased by moving the head, and is often relieved by 
venesection. 

The earlier stages of smallpox and pneumonia of the croupous 
type are often periods of violent headache, which symptom in the 
former instance decreases with the appearance of the rash, and in 
the case of croupous pneumonia so closely resembles the headache 
and associated symptoms of meningitis that a correct diagnosis, 
if the pulmonary signs are not sought for, may be difficult. In 
every case in which such symptoms occur the lungs should be 
examined; but it is possible for a meningitis due to the pneumo- 
coccus to be present without changes in the lungs. 

When headache is present in the course of croupous pneumonia 
it often lasts until crisis, but in some cases ceases by the third 
day. 

The chest should always be carefully examined in all cases of 
severe headache with fever for signs of pulmonary disease. 

Diffuse severe, but dull headache is a constant symptom in many 
cases of typhoid fever in the early stages, but the peculiar tongue 
(see chapter on Tongue), the tendency to diarrhea, the general 
systemic symptoms, and the facies of the patient will usually 
make its cause clear. More or less violent headache is often seen 
in measles, and depends* probably to a great extent upon the 
engorgement of the nasal mucous membrane, or, in other words, 
has the same causative factor as has an acute "cold in the head" 
in producing cephalalgia. 

Gruening is quoted by de Schweinitz as asserting that early 



VERTIGO 431 

morning headache is often due to nasal catarrh. This is, of course 
only true if digestive troubles, which are often due to alcohol, 
and renal disorders are excluded. Severe morning headache, or 
dull headache on first waking up, may be due to nocturnal attacks 
of epilepsy, of which the patient is ignorant. If the tongue is 
bitten or the bed wet with urine, this diagnosis receives strong 
support. 

Violent headache is often present during the febrile stage of 
intermittent fever and is often a complicating symptom of fever 
of the remittent type. In this connection the physician should 
remember that violent neuralgia of the supra-orbital nerve is 
sometimes due to malarial poisoning, and is called "brow ague." 

Headache or cephalic neuralgia is often due to anemia, whether 
it be the result of hemorrhage or of the deficient formation of 
blood. The pain is usually frontal; there are often giddiness on 
movement, palpitation of the heart, a peculiar sensation in the 
head, and pallor of the skin. An examination of the blood will 
usually reveal the cause to be in this tissue. 

Headache sometimes results from valvular heart disease. This 
is often associated with vertigo, stupor, sleepiness, and, as night 
approaches, a mild delirium may come on. Its probable cause is 
congestion or anemia of the brain. 

Rarely intracranial aneurysms produce headache, and when they 
are of the diffuse miliary variety this symptom may be a prodromal 
one before an attack of apoplexy. Large aneurysms may, however, 
exist without severe headache, and the position of the pain in no 
way indicates the seat of the aneurysm, save that aneurysm of the 
basilar artery may cause occipital pain. 

Headache may also arise from disease of the skull bones, either 
caries, osteitis, or periostitis, which result from injury, infection by 
syphilis or other infecting cause, such as typhoid fever or tubercu- 
losis; but there is nothing diagnostic about the headache in these 
cases save that it is generally most severe in the area involved, and 
pressure over that part may elicit more or less pain or tenderness. 

Violent neuralgia or shooting headache may be produced by 
exposure to cold, with resulting inflammation of the nerve sheath; 
by dental caries, and by middle-ear disease or disease in the external 
auditory canal. 

VERTIGO. 

Vertigo is a condition in which the patient feels as if he were 
losing his equilibrium. Sometimes he feels as if he were whirling 
around from right to left or left to right, sometimes as if falling 
forward or backward, and sometimes he seems stationary, while all 
his surroundings whirl around or rise up to or fall away from him. 



432 HEADACHE AND VERTIGO 

Although vertigo is a symptom which in itself lacks danger, it 
always produces great discomfort, if not fear. Functional vertigo 
arises from the patient being subjected to a whirling motion, from 
rough sea voyages, and from indigestion, deficient circulation, or 
excessive cerebral congestion. Often it is due to cerebral anemia 
arising from excessive hemorrhage or a feeble circulation. When 
it arises from indigestion it is probably due to reflex irritation, 
and perhaps to the absorption of toxic materials. 

Vertigo as a symptom has a far more serious significance when it 
arises from organic disease. The most common lesions which 
cause it are middle-ear disease, Meniere's disease, tumors of the 
cerebellum, of the pons, of the crura cerebri, and the corpora 
quadrigemina. Vertigo also is not only a premonitory sign of an 
epileptic attack, but in the epileptic state called petit mat or minor 
epilepsy it is often the only symptom. In persons with athero- 
matous arteries it is very common, and sometimes it is a persistent 
symptom for some days before an apoplectic seizure. It is also 
present in disseminated sclerosis. Finally, many drugs, such as 
quinine and the salicylates, may produce it. 

As the diagnostic points connected with most of the lesions here 
named are discussed elsewhere in this book, only Meniere's disease 
will be mentioned at this place. In addition to vertigo the 
characteristic symptoms of Meniere's disease are vomiting, noises 
in the ears, and, finally, deafness. The vertigo may be so severe 
that the patient falls to the ground. Aural examinations are 
usually futile in discovering any cause. Some authorities believe 
the disease to be due to a neurosis of the vasomotor nerves sup- 
plying the semicircular canals. 

A form of vertigo unknown in America, the paralyzing vertigo 
of Switzerland, described by Gerlic, is a paroxysmal vertigo with 
great loss of power in the limbs, partial ptosis, and preserved 
consciousness. 



CHAPTER XVI. 
COMA OR UNCONSCIOUSNESS. 

Coma is a condition of unconsciousness or insensibility from 
which the patient can be aroused but partially or not at all, and 
it may arise from injuries to the head, while the patient is in 
otherwise perfect health, which injuries produce laceration of the 
brain substance, cerebral or meningeal hemorrhage, or concussion. 
Again, it may be due to the influence of certain poisons, as alcohol, 
opium, chloral, cannabis indica, very large amounts of the bromides, 
or poisonous doses of other narcotics. Thirdly, it may arise from 
auto-intoxication, as in uremia, resulting from renal disease, 
and in cases of diabetes; in cases of profound exhausting disease, 
like typhoid fever or ulcerative endocarditis; or from acute yellow 
atrophy of the liver and pernicious malarial fever. Fourth, as a 
coincident symptom or sequel of hemorrhage into the brain (apo- 
plexy), as the result of an epileptic attack, of a cerebral embolism 
or thrombosis, of thrombosis of the cerebral sinuses, of cerebral 
abscess, of pachymeningitis, leptomeningitis, or cerebrospinal men- 
ingitis, of cerebral syphilis, of general paralysis, multiple sclerosis, 
and heat-stroke. The various points in connection with the 
diagnosis of coma from head injuries are to be found in surgical 
treatises, and the history of a head injury or the very presence of 
any injuries to the head is an important point to be sought after 
in the diagnosis. Care should be taken, however, to ascertain 
that any head injuries found to be present are not the result of a 
fall due to the onset of sudden unconsciousness, rather than the 
cause of the coma. 

Coma is sometimes seen as a later manifestation of Addison's 
disease, and it often develops very suddenly. 

Sudden unconsciousness may arise from heart failure due to 
disease or fright; we call this fainting. Frequent attacks of this 
character should cause the physician to listen to the heart to 
discover if there is valvular disease, particularly aortic regurgita- 
tion or mitral stenosis and fatty heart, and he should be on the 
outlook for renal difficulty. Sometimes sudden repeated attacks 
of unconsciousness are due to petit mat or minor epilepsy. Coma 
more or less profound follows attacks of true epilepsy. (See next 
chapter.) 

The coma of acute alcoholic poisoning is characterized by pro- 
28 



434 COMA OR UNCONSCIOUSNESS 

found insensibility, great muscular relaxation, loss of the ocular 
reflexes, and great fulness of the bloodvessels of the neck and face 
in the early stages, and, finally, by ghastly pallor of the face as the 
coma deepens on the approach of death. The skin is moist and 
warm at first, but afterward becomes cold. The pupils are usually 
moderately dilated; the pulse is rapid, at first strong, then more 
and more feeble, and the respiration stertorous and heavy. The 
sphincters, as a rule, are not relaxed, although they may be so in 
rare cases. The bodily temperature in severe alcoholic poisoning 
progressively falls from i° to 6° F. below normal. 

Alcoholic coma is to be separated from that due to opium poisoning 
by the absence of the contracted pupils and slow breathing of the 
latter condition, in addition to the other symptoms named below 
in discussing that condition; from coma due to cranial fracture by 
the absence of any history or sign of head injury; 1 from chloral 
poisoning by the history, the greater fall of body temperature, and 
the great feebleness of the heart and respiration produced by chloral. 
It may be impossible to separate alcoholic poisoning from that of 
cannabis indica poisoning except for the fairly strong pulse gener- 
ally found in the latter condition, and the history of the patient 
having taken the hemp or complained of the peculiar sense of 
prolongation of time before the coma came on. 

The symptoms accompanying the coma of opium poisoning are 
heavy sleep, preceding the deep unconsciousness, during which the 
patient can usually be aroused by shouting in his ear or by violent 
shaking, but sinks back into slumber at once on being undisturbed. 
The face is suffused and reddened and may be finally distinctly 
cyanotic, and the breathing is puffing and stertorous. When the 
patient is awakened he breathes more rapidly, and for this reason 
the duskiness of the face disappears and the normal hue returns. 
Death never occurs in the second stage of opium poisoning from 
the poison alone; but, if disease is present, death may take place 
at this time. The pupils are contracted to pin-points. The third 
or fatal stage emerges from the second by a gradual process, so 
that no abrupt line of separation can be noted. The face becomes 
at first more cyanotic, then pale and livid; the respirations, which 
have been 8 to io in the minute, are now only 4 or 5; and, finally, 
such prolonged pauses occur that all hope of another respiration 
is lost by the attendant. While the slow breathing is at first deep, 
it now rapidly becomes shallow, and relaxation is present to the 
greatest degree. The skin, previously dry, is wet with the sweat 
of death; the patient is so deeply narcotized that nothing can 
arouse him, and he dies from respiratory failure, although the 
heart ceases almost simultaneously from the asphyxia. The 

1 The physician must not forget that a fall from alcoholism may result in a 
cranial fracture. 



COMA OR UNCONSCIOUSNESS 435 

pupils do not dilate in the third stage, except in the relaxation of 
death. 

In view of the frequency with which alcohol and opium poison- 
ing are confused, the following table is appended, which will be 
found of value in making a differential diagnosis as to the condi- 
tion of the patient: 

Opium poisoning and Alcoholism. 



Opium-poisoning. 

1. Pupils contracted. 

2. Respiration and pulse slow and full. 

3. Face suffused and cyanosed. 

4. Skin warmer than in alcoholic poisoning. 

5. Pulse slow, strong, and full till late in 

poisoning. 



Alcoholism. 

1. Pupils normal or dilated. 

2. Respiration nearly normal ; pulse rapid, 

and finally feeble. 

3. Pace may be pallid. 

4. Skin cool, perhaps moist. 

5. Pulse rapid, at first strong, then weak. 



There is scarcely any difference as to consciousness in these 
two conditions. 

When a poisonous dose of chloral is taken the person soon falls 
asleep and then sinks into a deep coma. The respirations become 
at first slow and labored, then shallow and feeble. The pulse, 
at first perhaps a little slowed, soon becomes rapid, thready, and 
shuttle-like, and is finally lost at the wrist. The face is white 
and livid, the forehead and the hands covered with a cold sweat, 
and the pupils, which are at first contracted, soon become widely 
dilated. Absolute muscular relaxation is present, and it is impos- 
sible to arouse the patient. 

The coma of uremia may come on gradually, but most commonly 
its onset is sudden and it may or may not follow a uremic con- 
vulsion. It possesses no diagnostic sign or signs which clearly 
separate it from the unconsciousness or coma following epileptic 
attacks, and, as the uremic convulsion is often typically epileptic 
in character, the differential diagnosis is very difficult. An examina- 
tion of the urine, if it can be obtained by the catheter or otherwise, 
will indicate, but not prove, the presence of uremia if albumin be 
found in either large or small amounts, and the presence of very 
little urine in the bladder, indicating anuria, may be of some 
diagnostic significance. On the other hand, if the uremia be due 
to chronic contracted kidney, the urine may be plentiful, the 
albumin scanty, but the low specific gravity is noteworthy. The 
pulse is usually very slow, often but 40 to 50, but the arterial 
tension is high, so that the artery feels hard and unyielding. The 
temperature of the body is usually very low in those severe cases 
which are free from convulsions and have a progressively down- 
ward course; so low a point as 91 ° to 95 is sometimes reached. 
at which time the patient is usually moribund from collapse. 
When convulsions are present the temperature may rise as high 
as 108 , and there may be in some cases a severe chill, followed 



436 COMA OR UNCONSCIOUSNESS 

by fever, and this again by collapse. The respiration is nearly 
always very deep, and sometimes very much quickened, and at 
times has a peculiar hissing sound. Sometimes the patient may 
purse his lips as if to whistle. Cheyne-Stokes breathing may be 
present. Rarely the breathing is difficult and asthmatic in type 
(uremic asthma). If a preceding history of prolonged nausea, 
attacks of colliquative diarrhea, and vertiginous symptoms can be 
discovered as having been present prior to unconsciousness, these 
will add to the array of uremic probabilities. The coma of uremia 
is not necessarily a fatal symptom. Even in very severe cases 
remarkable recoveries sometimes occur. 

Coma resulting from diabetes mellitus is of far graver import, as 
it commonly terminates the patient's life. There may not be any 
prodromes, and there may not be any history of an exciting cause 
for the coma in a case of diabetes. Sometimes it is provoked in 
patients by severe exercise or great mental strain or emotion. 
When unconsciousness does not come on at once, the patient, after 
suffering from nausea, headache, and respiratory oppression, 
suddenly becomes anxious, delirious, and violent, then drowsy and 
deeply comatose. The pulse is not particularly noteworthy, but 
is usually full and not very tense. The respirations are deep and 
often very noisy, but at about the normal rate, although some- 
times they may be rapid in the condition called diabetic dyspnea. 
The body temperature falls very greatly, even below 90 ° F. The 
respiratory changes and those in temperature may, therefore, be 
very much like those of uremia; but in association with the coma 
of diabetes mellitus there are two pathognomonic symptoms: 
first, the sweet odor of the breath, which smells like the aroma of 
a pear or an apple, or a faint odor of chloroform; and, second, the 
presence of sugar in the urine. Testing for acetone usually reveals 
it in the urine in excess. 

Ordinarily coma is rare in typhoid fever, and when it occurs is 
due to some complication, such as abscess or effusion at the base 
of the brain or meningitis; it is usually replaced by what is called 
" coma-vigil," in which the patient, in a semiconscious state, keeps 
muttering day or night. This is a grave sign. 

The coma of acute yellow atrophy of the liver, a very rare disease, 
is generally preceded by headache, nausea, anorexia, and perhaps 
fever, followed by nervous excitement or restlessness, and then 
mental hebetude, which is often accompanied by a noisy delirium 
which may amount to mania. Finally, after several days, coma 
comes on and gradually becomes more and more profound until death 
takes place. Some of these symptoms resemble those of uremia 
or diabetic poisoning, but the coma of acute yellow atrophy has 
in addition these characteristic signs, namely, jaundice, bile- 
stained urine, marked shrinking of the liver dulness, enlargement 
of the spleen, and hemorrhages into the skin, or these effusions 



COMA OR UNCONSCIOUSNESS 



437 



may take place into the bowels and stomach. The urine is singu- 
larly free from urea, but contains leucin and tyrosin in large 
amounts. Acute yellow atrophy of the liver is so very rare that 
this disease may be excluded by the law of probabilities. 

When coma comes on as the result of pernicious malarial infec- 
tion, it is most apt to be ascribed to sunstroke, uremia, or apoplexy, 
for its onset is usually sudden. Only a history of exposure to 
malarial influences, the presence of slight jaundice and anemia, 
and of an enlarged spleen will serve to separate it from these 
conditions, and an examination of the blood for the malarial 
organism may be necessary before a positive differentiation can 
be made, for the diagnosis is by no means easy. 

The coma of apoplexy may be sudden or gradual in its onset; 
generally it rapidly appears after the first symptoms of cerebral 
hemorrhage develop. The loss of consciousness may be partial 
or absolute, generally the latter if the leakage from a ruptured 
vessel be great. The respirations become stertorous, generally 
more rapid than normal, and, if a fatal result is in prospect, are 
rhythmically irregular; that is, they are now very slow, then gain 
in speed gradually until they become very fast, then the speed 
and vigor gradually fall until they are as feeble and slow as before 
(Cheyne-Stokes respiration). The history of preceding paralysis 
on one side of the body, or the presence of this loss of power if it 
can be demonstrated, the unequal pupils, the drawing of the face 
away from the paralyzed side, a strong, bounding pulse, and gener- 
ally raised temperature complete the clinical picture of the coma 
of cerebral hemorrhage. If death does not ensue, consciousness 
may return, and the patient progress to recovery; but sometimes 
after several days of apparent convalescence a secondary fatal 
irritative coma comes on, associated with high fever. This is 
usually of ominous portent and is readily recognized because of 
the history. (See chapters on the Arms and on the Legs and on 
Hemiplegia.) 

The coma of cerebral hemorrhage is unfortunately often taken for 
acute alcoholism, particularly as the latter state often induces the 
hemorrhage. The following table is designed to separate them: 



Acute Alcoholism and Apoplexy. 



Alcoholism. 

1. Pulse rapid, compressible, and weak. 

2. Skin moist, or relaxed and cool. 

3. Bodily temperature lowered. 

4. Pupils equally contracted or dilated ; gen- 

erally dilated. 

5. No hemiplegia. 

6. Breathing not so stertorous nor so one-sided 

in lips. 

7. No facial palsy. 

8. Unconsciousness may not be complete. 



Cerebral Hemorrhage. 

1. Pulse apt to be strong and slow. 

2. Skin hot or dry. 

3. Bodily temperature raised. 

4. Pupils unequal. 

5. Hemiplegia ; one side tossed, the other re- 

maining motionless 

6. Respiration stertorous, the lips being in- 

flated on one side on expiration. 

7. Facial palsy. 

8. Unconsciousness complete. 



43& COMA OR UNCONSCIOUSNESS 

The smell of alcohol in the breath is no guide, as the acute 
alcoholism may have caused the rupture of a cerebral blood- 
vessel. 

Coma due to cerebral softening, following embolism or throm- 
bosis, has no signs other than those discussed in the diagnosis of 
these lesions in connection with hemiplegia (which see). Coma 
due to thrombosis of the sinuses of the brain is accompanied by the 
following diagnostic symptoms, namely, irritation or paralysis of 
the cranial nerves resulting in strabismus, nystagmus, and lockjaw, 
stiffness of the neck, and clonic spasms. If the cavernous sinus is 
thrombosed, there will generally be found stasis of the veins in the 
eye, which means retinal congestion. The eyeball may be pro- 
truded, the eyelids swollen, and perhaps loss of function in the 
oculomotor nerve may be present, causing ptosis, and, if the 
abducens is affected, causing internal strabismus from paralysis 
of the external rectus. If the transverse sinus is involved, there 
will probably be edema behind the ear, and, if the petrosal or 
internal jugular be obstructed, the proximal part of the vein 
collapses. Thrombosis of the superior longitudinal sinus causes 
epistaxis and engorgement of the temporal veins. Thrombosis of 
any of these sinuses, however, may be present without these signs. 

Coma due to subdural hemorrhage (pachymeningitis interna 
hemorrhagica) is peculiar in the fact that its onset is usually very 
slow, and the signs of nervous irritation last a long time and are 
quite violent, often amounting to epileptic paroxysms. Commonly, 
too, there will be rigidity of one limb, but the cranial nerves usually 
escape. The coma usually fellows' these signs, and the condition is 
peculiarly common in the chronic insane and in paretic dements. 

Sudden unconsciousness with hemiplegia and vomiting may also 
come on in Raynaud's disease. 

Coma from cerebral abscess is accompanied by symptoms closely 
resembling those of acute meningitis. The patient is dull and 
delirious; has headache, fever, and often has a hyperpyrexia. The 
sensibility becomes less and less, and deepens into the coma which 
ends in death if relief is not given. The localizing symptoms of 
paralysis may indicate that a lesion is in a certain part of the brain; 
but generally these signs are absent, because cerebral abscess is 
usually in the frontal lobes. If there is a history of injury, purulent 
otitis, infectious disease involving other parts, such as septicemia 
from wounds or empyema, and if there are vertigo, vomiting, and 
headache, fever, and an absence of choked disk of the optic nerve, 
the diagnosis is probably cerebral abscess; but a long duration of 
months is no sign that it is not abscess, as these cases often run 
a very prolonged course. (See chapter on Headache.) 

The coma of purulent leptomeningitis resembles that of abscess in 
many of its associated symptoms; but the intense headache, the 



COMA OR UNCONSCIOUSNESS 439 

rapid development of delirium and unconsciousness, the stiffness 
of the neck, the optic neuritis and disturbed movements of the 
ocular muscles, combined with the absence of a history of septic 
absorption, may make a differential diagnosis possible. Purulent 
leptomeningitis is rare, but it sometimes occurs in association with 
croupous pneumonia, and the presence of this disease will point to 
the cause of the coma. 

The coma due to epidemic cerebrospinal meningitis is diagnosti- 
cated by the characteristic rigidity of the neck, excessive headache 
preceding the unconsciousness, the disturbances of the cranial 
nerves producing strabismus, unilateral or bilateral ptosis, nystag- 
mus, impaired pupillary reaction, mydriasis, and myosis. The face 
is often painfully distorted. The presence of an epidemic, of 
course, makes the diagnosis clear. (See chapter on Headache.) 

It is well to remember that coma may be present from other 
forms of meningitis and arise in several conditions presenting 
similar symptoms, such as pneumonia of the meningeal type, 
otitic abscess, and gastro-enteritis. (See chapter on Headache 
and Vertigo.) 

Cerebral syphilis may result in the development of coma by 
producing hemorrhage, embolism, arteritis, tumor of the brain, or 
almost any other lesion, and its diagnosis as the cause of an attack 
of coma is not easy. Of course, a history of syphilitic infection 
and the presence of symptoms of this condition in a patient who 
is too young to have secondary arterial changes from age render 
the probability of syphilis as a cause very great. Scars on the skin 
(see chapter on the Skin) may show specific taint. 

When coma results from general paralysis it usually succeeds the 
peculiar epileptic attacks which come on late in that disease, and 
the history of delusions, tremor of the hands, peculiar speech, 
loss of the reflexes, with earlier milder attacks, like the one before 
us, combined with the age of the patient, render a diagnosis 
possible. 

Practically identical symptoms may attend the development of 
coma from multiple sclerosis, and without the history of the latter 
affection the diagnosis may be impossible. If this history shows a 
spastic gait and intention tremor, nystagmus, mental weakness, 
and heightened reflexes, the probability of the attack being due 
to multiple sclerosis is increased. 

Heat-stroke produces coma as one of its most constant symptoms. 
The history of exposure to heat and the hyperpyrexia are the two 
diagnostic points of importance. (See Fever.) 



CHAPTER XVII. 
CONVULSIONS OR GENERAL SPASMS. 1 

Definition of a convulsion — The convulsions of epilepsy in its various forms — 
Of infancy — Of hysteria — Tetanic convulsions — Tetany — Chorea. 

A convulsion is a condition in which be reason of sudden tonic 
or clonic contractions of groups of muscles the body in whole or in 
part is thrown into spasmodic movements. Convulsions can be 
divided into those which are clonic or epileptiform and those 
which are tonic or tetanic. Further, it is a general rule that con- 
vulsions which are epileptiform or clonic in character have their 
origin in the cerebral cortex, while those of the tetanic or rigid 
type arise from excitation of the motor tracts in the spinal cord. 
The clonic variety of convulsions are represented by idiopathic, 
traumatic, reflex, and syphilitic epilepsy, hysterical convulsions 
of an epileptic type, uremic convulsions, and those convulsions 
which arise from the presence of growths or other sources of irri- 
tation in the cerebral cortex. Certain poisons may also rarely 
produce such attacks, notably lead and alcohol, and sometimes 
malingerers imitate very successfully the epileptic paroxysm. 

The convulsion in epilepsy is characterized in some cases by the 
primary appearance of an aura — that is, a sensation in some part of 
the body, which the patient discovers comes on before each convul- 
sion. This aura may be of any character and appear in any part. 
Most commonly it is sensory, and is as if a cloud or wave were 
passing up the body to the head. As the sensation reaches the 
head the patient may utter the peculiar epileptic cry or sigh, 
and with this sound the body becomes rigid from tonic spasm of 
the muscles. This spasm now relaxes for an instant, and then 
the patient's muscles pass into a state of alternate relaxation and 
contraction which throws the patient's body from one place to 
another. 

The primary tonic spasm of the face produces risus sardonicus in 
some cases: the head is often drawn to one side, the eyes commonly 
turned to the same side, and the lower jaw locked tightly against 
the upper jaw. The arms are strongly flexed at the elbows, the 

1 For local spasms or tremors, see chapters dealing with the Face and Head, 
Hands and Arms, and Feet and Legs. 



CONVULSIONS OR GENERAL SPASMS 44 1 

hands flexed at the wrists, and the fingers bent into the palms of 
the hands with great force. As a rule, the evidence of the powerful 
flexors overcoming the extensor muscles predominate; but some- 
times the reverse is the case, and forcible, rigid extension of the 
parts affected takes place. The duration of these tonic contrac- 
tions rarely exceeds two minutes, and in most cases is limited to 
but a few seconds. 

The state of spasm is followed by clonic spasms, which are ushered 
in by more or less violent tossings, but whose onset is forewarned 
by peculiar vibratory thrills which run through all the affected 
muscles. The eyelids tremble, the body changes its position 
never so slightly, and then, as if the vibrations gained greater and 
greater power with each movement, the fibrillary tremors give way 
to muscular contractions. The expression of the face, which in the 
preceding state was set and firm, is now constantly changed by the 
movements of the facial muscles; the jaws, no longer locked together 
are gnashed and crunched one upon the other; the tongue is alter- 
nately protruded and drawn back, and, as a consequence, is often 
caught between the teeth and lacerated. The excessive movements 
of the muscles of mastication force the increased quantities of 
liquid secreted by the salivary glands from the mouth in the form 
of froth, which is often stained with blood by reason of the injuries 
of the tongue. The constancy of the convulsive movements now 
becomes less and less marked; well-developed remissions occur 
between each toss of the body until the movements cease entirely; 
but it should be constantly borne in mind that the prolongation 
of the remissions does not produce any decrease in the severity 
of the intervening spasm, the final spasm often being even more 
violent than the first. 

The intense discoloration of the face begins to pass away as soon 
as the remissions, by their length, permit the blood to be oxygenated, 
its disappearance being temporarily arrested by each paroxysm. 
Finally, the spasms having ceased, the patient lies before us 
relaxed, unconscious, and exhausted, and usually passes into a 
deep sleep or coma, which lasts a variable length of time, and from 
which he cannot be aroused, except very rarely, and then with 
great difficulty. 

When one part of the body is involved in an epileptic paroxysm, 
the rest of it escaping, the condition is called Jacksonian epilepsy. 
By far the most important of its peculiar signs is the character of 
the onset, which always begins, in the typical Jacksonian form, in 
some peripheral portion of the body, and most frequently in the 
muscles of the thumb or hand, so that for the moment the con- 
vulsive movements are localized. They may remain localized at 
the point of origin, or immediately diffuse themselves over muscle 



442 CONVULSIONS OR GENERAL SPASMS 

after muscle until all the arm, leg, or other groups of muscles are 
involved. It is of the greatest importance, however, that the 
reader should keep the aura of an attack separate in his mind 
from the onset, remembering that the term onset is here used to 
designate the beginning of the period following the aura, if there 
be one. 

Jacksonian epilepsy may be of almost any severity. In rare 
cases only one muscle may suffer throughout an entire attack, 
but in others the entire body may be at last convulsed. There 
may or may not be loss of consciousness, its presence or absence 
being dependent upon the seat of the lesion in the brain and the 
severity of the attack. In those instances in which only a few 
localized muscles are involved consciousness is more commonly 
preserved than lost. 

Typical Jacksonian epilepsy may develop in the course of general 
paresis. 

An epileptiform convulsion may be associated with the onset of 
an apoplexy, and usually indicates that the hemorrhage is in the 
motor cortex. Such an attack is generally Jacksonian in character; 
that is to say, one muscle or a group of muscles is involved, or, if 
not this, the attack is, at most, only unilateral. The cause is made 
manifest by the presence of the symptoms of apoplexy as generally 
seen, for there are inequality of the pupils, drawing of the face to 
one side, and a consequent hemiplegia which lasts indefinitely. Of 
the attack itself, it may be said that, so far as the movements are 
concerned, they differ in no way from those of the true Jacksonian 
epileptic seizure; and it should be remembered that hemiplegia 
often follows ordinary idiopathic epilepsy. Such a postepileptic 
hemiplegia is, however, usually fleeting, while that due to hemor- 
rhage is more or less permanent. It should be remembered, how- 
ever, that apoplexy may complicate epilepsy, being produced by 
the convulsions. Then, again, the lesions caused by a hemorrhage 
may ultimately result in epileptiform attacks, although this is 
certainly rare in adults. In some persons the history of this 
hemorrhage is very indistinct, owing to its occurrence in early 
life; while in others the paralysis has been so slight or temporary 
as not to bear any relation in the mind of the patient with the 
convulsive seizures following, which in many cases do not occur 
for some time after. The palsy and convulsions are not always 
due to hemorrhage, but to any pathological cerebral change. 
Heart disease, by causing embolism, may bring them on, and 
syphilis and puerperal sepsis may all produce a softening of the 
cortex, with an epileptic state following the paralysis. 

We can very readily divide posthemiplegic epilepsy into two 
classes, for we find that in about one-half of the cases the convulsion 



CONVULSIONS OR GENERAL SPASMS 443 

occurs along with the paralysis and then follows at intervals, while 
in the other half the paralysis is not followed by convulsive seizures 
for weeks, months, or years. 

Posthemiplegic epilepsy may occur at any age, but there can be 
no doubt that it far more commonly occurs in children than in 
adults. In at least two-thirds of the cases the onset is before five 
years of age, and in nearly one-half it is during the first two years 
of life. 

The convulsions may occur along with the first attack of par- 
alysis, and continue, or that an interval may occur between the 
attack and the subsequent paroxysm. The chronic recurrent fits 
date from the onset in about one-third of the cases, but it is not 
uncommon for the paralysis to occur in infancy and the epilepsy 
to begin at puberty. It would seem that cells injured in early life 
may lie undisturbed until the increased demands of maturity 
call them out into diseased action. This prolonged interval occur- 
ring so commonly in children separates them from adults in this 
disease, for in this latter class it is very rare for the epilepsy to be 
delayed for more than one year. 

Syphilitic epilepsy is only one of the many nervous affections 
which afflict those who may be so unfortunate as to contract this 
disease. There can be no doubt that syphilis produces epilepsy 
in adults. 

There is also one symptom which may occur early in syphilitic 
epilepsy, or sometimes only late in the disease, namely, repeated 
partial, passing palsies, which while they may be in some cases 
hysterical, are in the syphilitic almost pathognomonic of brain 
involvement — a momentary weakness in one arm; a slight draw- 
ing of the face to one side, which appears in a few hours; a tem- 
porary dragging of the toe; a partial aphasia which appears and 
disappears; a squint which tomorrow leaves no trade behind it. 
(See Syphilitic Arteritis.) 

It is important to determine whether idiopathic epilepsy can be 
separated from that due to syphilis simply by the symptoms. This 
is very difficult to decide. So far as the convulsion itself is con- 
cerned, it is not possible to separate them. If, however, we can 
obtain any history, the matter becomes much more simple. 

Fournier says: 

i. In syphilitic epilepsy there is nearly always absence of the 
shrill cry at the onset, so characteristic of the idiopathic variety. 

2. There is frequently paralysis immediately after the attacks. 

3. The seizure is incomplete or unilateral in character. 

4. Attacks constantly increase in severity. 

Epileptic convulsive disorders may arise owing to the action 
of a very large number of toxic substances, of which only a few 



444 CONVULSIONS OR GENERAL SPASMS 

will be considered here, as an enumeration of all of them is mani- 
festly impossible. 

Alcoholic epilepsy consists of two distinct varieties produced by 
overindulgence in intoxicating drinks. In one of these the convul- 
sions are symptomatic of acute poisoning, and come on during a 
drunken orgy or immediately after a single large draught of liquor. 

In the second variety the convulsion does not originate while 
there is alcohol in the blood, but in the intervals between the attacks 
of dehrium tremens resulting from chronic excessive alcoholic 
indulgence. Under these circumstances the paroxysms are gener- 
ally accompanied by hallucinations or by dementia or imbecility. 
In the alcoholic convulsion the symptoms may closely resemble 
those of true epilepsy, and not rarely the attack is ushered in by 
headache, gastric disturbance, disorders of vision, and excessive 
tremors or some similar prodrome which may be looked upon as 
partaking of the nature of an aura. As a general rule, these alco- 
holic convulsions occur in paroxysms — two, three, four, or more, 
one after the other, at intervals of a few minutes. Not only may 
grand mal be closely simulated by alcoholic epilepsy, but simple 
vertigo or true petit mal may exist, either alone or associated with 
major convulsions. Alcoholic epilepsy is often associated with 
hallucinations, especially of terror, and not rarely is followed for 
days by a certain degree of mental disturbance. Rather curiously 
these cerebral disturbances result rather in suicidal than homicidal 
tendencies, which is just the reverse of the insanity following 
simple epilepsy. 

The symptoms of a uremic convulsion will be spoken of further 
when studying its differential diagnosis in connection with epilepsy. 

The diagnosis of lead epilepsy from the idiopathic varieties is 
somewhat difficult, if the patient is seen for the first time during 
an attack; but the ordinary methods of determining chronic lead 
poisoning are, of course, of equal value here. The blue fine on the 
gums may be present, and, if so, the diagnosis is almost certainly 
lead poisoning; but its absence is no proof that lead is not present. 
The administration of iodide of potassium also will so increase the 
elimination of the poison as to benefit the case and render it more 
easy to recover lead from the urine. 

The history of exposure to lead in any form is, of course, exceed- 
ingly valuable evidence, but it should not be forgotten that in many 
cases this history is wanting. Amaurosis may be present in some 
cases, or optic neuritis with atrophy may occur. Where double 
wrist-drop is present the diagnosis is much more easy. 

The symptoms of epilepsy due to chronic poisoning by lead are 
chiefly as follows: the man, apparently in his usual health, or who 
has had for a few days a feeling of weight in the head, or headache, 



CONVULSIONS OR GENERAL SPASMS 445 

is suddenly seized with most violent convulsions, which are often 
fatal, and which during their presence resemble ordinary epilepsy 
so closely as not to be separated from it. They end in coma, and 
are separated from each other by intervals of nervousness and 
disquiet. In some cases one convulsion follows the other so rapidly 
that death ensues from exhaustion, but in much more rare instances 
the attacks may resemble Jacksonian epilepsy very closely, and 
there may be no loss of consciousness. If such a condition occur, 
it is almost sure to be followed by a more violent fit. The attacks 
are not preceded by any aura whatever, but previous to the head- 
ache, already mentioned, the patient may have had amaurosis, 
and ophthalmoscopic examination of the eyes may show choked 
disk and neuritis of the optic nerve. As a general rule, such cases 
are fatal, but they may recover under careful treatment. 

It is exceedingly important to differentiate between those con- 
vulsions which arise from uremia brought on secondarily by an 
action of lead on the kidneys and those which are due to a direct 
action on the brain. This may be difficult from the mere symptoms 
presented, but there are some points of difference. In the first 
place, the convulsion of uremia is, as a general rule, not so violent 
in its movements nor so sudden in its onset. It is generally pre- 
ceded by a few days of somnolence, or weeks of gastric disorder 
and headache, while lead epilepsy is generally sudden or preceded 
by cephalalgia by only a few days of hours. 

Epilepsy very closely resembles hysteria, and the diagnosis of 
one from the other is as difficult in some cases as it is essential 
and necessary for treatment and cure. 

As already stated, in epilepsy the movements are typically at 
variance with those of daily life, while in hysteria they are almost 
equally typical of ordinary muscular contractions, or, in other 
words, are more purposive in character, and frequently there is 
prolonged tonic contraction of the muscles, giving rise to the 
assumption of positions which bear more or less resemblance to 
normal attitudes. In hysteria, also, consciousness is impaired 
sometimes, but never so completely as in true epilepsy. Indeed, 
most commonly the individual knows all that goes on around her, 
for, while she may give no sign of consciousness by words or looks 
during the attack, she may afterward be able to narrate all that 
has occurred. Less commonly in hysteria, a condition known as 
automatic consciousness exists, in which, during the paroxysm, 
the patient understands all that is said, but forgets everything 
on the return to quietness. 

The other conditions with which it might be confused are uremia, 
alcoholic epilepsy, tetanus, and syncope. Below are arranged all 
these disorders in a table, which briefly shows the different points 
between them. 



446 



CONVULSIONS OR GENERAL SPASMS 



Table of Differential Diagnosis of Epilepsy from Hysteria, 1 etc. 



Signs. 


Epilepsy. 


Hysteria. 


Uremia. 


Petit mal. 


Alcoholic 
epilepsy. 

None. 


Tetanus. 


Syncope. 


Apparent 


None. 


Emotion. 


None. 


None. 


None. 


Mental 


cause. 














shock. 


Aura or 


Generally 


Globus 


Headache, 


Faintness 


Tremors. 


Nervous- 


Not so well 


prodro- 


present, 


hystericus: 


vomiting, 


and dim- 




ness. 


defined as 


mas. 


but short. 


palpitat'n; 
choking. 


and dys- 
pepsia. 


ness of 
vision. 






in epilepsy. 


Onset. 


Sudden. 


Often 


Often 


Sudden. 


Sudden or 


Gradual; 


Sudden or 






gradual. 


gradual. 




gradual. 


begins 


gradual. 


Scream. 


At onset 


During 


Frequently 


Frequently 


May or may 


in jaw. 
None. 


None. 




and sud- 


attack. 


none. 


none. 


not be 








den. 








present. 






Convul- 


First tonic, 


Rigidity 


Rigidity 


No rigidity. 


Movement 


Always 


None. 


sion. 


then 


more pro- 


generally 




more clonic 


tonic. 






clonic. 


nounced, 

with more 

aching. 


absent. 




than tonic. 






Biting. 


Tongue. 


Rarely. 


Tongue. 


None. 


Rarely. 


None. 


None. 


Micturi- 


Frequent. 


Never. 


Never. 


Rarely, ex- 


Rarely. 


Some- 


Never. 


tion. 








cept when 
bladder is 
affected. 




times. 




Defecation. 


Occasion- 
ally. 


Never. 


Never. 


Never. 


Rarely. 


Rarely. 


Never. 


Talking. 


Never. 


Frequent. 


Muttering. 


Never. 


Never. 


Never. 


None. 


Duration. 


A few 


Generally 


From a 


Momen- 


May be 


Hours. 


Indefinite. 




minutes. 


many 
minutes. 


minute 
to hours. 


tary. 


prolonged. 




time. 


Conscious- 


Lost. 


Generally 


Lost. 


Not lost 


Lost. 


Pre- 


Lost. 


ness. 




preserved. 




always, but 

clouded. 

Spontane- 




served. 




Termina- 


Spontane- 


May be in- 


Spontane- 


Spontane- 


Sponta- 


Gradual, 


tion. 


ous. 


duced by 
shock. 


ous. 


ous. 


ous. 


neous. 


with no 
somnolence 



The movements of the hysterical patient after the tonic con- 
dition has passed away are as clonic as those of the epileptic, but 
still possess some purposive characteristics, and are not so bizarre 
as are those of the true disease. Thus the head, arms, and legs 
are struck with evident endeavor against the floor or surrounding 
furniture. Another point, which, when it occurs, is very distinctive, 
is the onset, toward the close of an hysterical convulsion, of a 
second stage of tonic spasm, such as occurred at the beginning. 
It will be remembered that this does not occur in epilepsy, although 
it must be borne in mind that in cases of the "status epilepticus" 
the rapid onset of another attack may show a second tonic stage. 
This can be separated, however, by the fact that it is followed 
by clonic movements, whereas the secondary tonic stage of hysteria 
is usually followed by relaxation and temporary recovery. 

In the secondary hysterical tonic contractions, emprosthotonos 
and opisthotonos may occur, and are even more rigid in their 
character than they are in the first attack in some cases. Finally, 
too, in hysteria some peculiar emotional position is often assumed, 



1 This table is taken from the author's essay on Epilepsy, a prize essay of the 
Royal Academy of Medicine in Belgium, January, 1889. 



CONVULSIONS OR GENERAL SPASMS 447 

as of the crucifix or of intense grief, or, perhaps, immoderate 
laughter is indulged in, with corresponding movements of the 
trunk. If the patient is quiet at this time, a smile may float across 
the face, while the eyes, with a look of pleasure, pain, or entreaty, 
may seem to be gazing at some object very far off. In some very 
well-developed cases the expression of pleasure is followed by a 
look of pain, with painful movements, or an appearance of intense 
voluptuous entreaty, with sensual venereal desire evidenced by 
gestures. Great terror may be present, and, as the scene constantly 
changes, the woman is now joyous, now mournful, now scolding, 
now praising her attendants or herself. Such is the history of a 
fully developed attack of hysteria. 

In France there can be no doubt that the tongue is commonly 
bitten in hysterical convulsions, and that frothing of the mouth is 
frequently present; but in other countries this symptom may be 
regarded as indicative of epilepsy rather than hysteria. 

If a large number of patients suffering from these hysterical 
attacks be questioned between times, it will be found that the so- 
called globus hystericus becomes an almost constant precursory 
symptom of an attack; and if the relatives be questioned, it will 
often appear that they have noticed that the fall to the floor is 
more gentle than in true epilepsy; but this is not always so by any 
means. Again, the expression of the face in hysteria is, between 
the attacks, often very characteristic, and the surrounding atmos- 
phere of the patient seems, even to the inexperienced, to breathe 
hysteria. Very commonly areas of anesthesia and hyperesthesia 
occur in these patients, and are of all degrees of intensity and 
limitation. Search for them generally shows their presence after 
attacks of convulsions, but they may exist from one attack to 
the other, or develop spontaneously. In nearly all cases these 
areas are unilateral, and may extend entirely over one-half of the 
body, the line of demarcation of the anesthesia or hyperesthesia 
from the sound area being clearly and abruptly defined, generally 
at the median line of the front and back of the trunk. (See chapter 
on the Skin, that part dealing with Anesthesia.) It will be called 
to mind that such conditions are very rare in true epilepsy. Hal- 
lucinations are far more common after the fit in hysteria than in 
epilepsy, and sometimes they even occur during the attacks. The 
pupil is more mobile in hysteria than in epilepsy, but may be 
contracted, normal, or widely dilated. 

The following table gives, in as brief a manner as possible, the 
differentia] diagnosis between epilepsy and hystero-epilepsy, and 
is founded on a lecture by Professor Charcot, delivered at the 
Salpetriere: 



448 CONVULSIONS OR GENERAL SPASMS 



True Epilepsy. 

Aura short. 

Cry is violent. 

Spasms first tonic, then clonic, then followed 
by stertor. 

Sometimes after fit of delirium or violent im- 
pulse or mania. 

Mental power is lost. 



Hystero-epilepsy. 

Aura extremely prolonged. 

Cry is more moderate and prolonged. 

Ataxic contractions, extension of limbs, turn- 
ing of head, clonic movements, slight stertor. 

Bizarre contractions, no delirium, may be 
hallucinations. 

Mental power preserved. 



No emotional attitudes. ' Emotional attitudes. 

A differential point, strongly insisted upon by Charcot and 
Bourneville, is that in true epilepsy there is generally a very 
considerable rise of temperature during an attack, while in hystero- 
epilepsy the temperature remains normal or is only slightly raised. 

Finally, in the diagnosis of true epilepsy from convulsions of a 
hysteroid character it is well for the physician to remember that 
the proportions of the two conditions in frequency of occurrence 
is, according to Gowers, 815 to 185 in every 1000 cases. 

The differentiation of epilepsy from uremia is more readily 
made, for there is usually a previous history of symptoms pointing 
to renal trouble, as, for example, somnolence, or mental apathy, 
for some days or hours before the attack. Of course, in such cases 
recourse may be had to the ordinary tests for such conditions of 
the urine as are generally found when uremia exists ; but it is to be 
remembered that epilepsy and kidney, disease may exist hand in 
hand, and that for this reason the prognosis and diagnosis are to 
be carefully formed and given. If in a given case a prolonged 
history of dyspepsia, of frequent vomiting, occasional attacks of 
dyspnea, and failure of general health is found to be present, the 
correct diagnosis probably will be uremia. The preservation or loss 
of consciousness in uremic convulsions is variable. Generally, if 
the convulsion is widespread and severe, the intellection is lost; 
but if it be only a slight attack, consciousness may be preserved. 
So long ago as 1840, Bright described cases of uremia, on the 
other hand, in which violent convulsions occurred without loss 
of consciousness, and Roberts has reported similar instances. 

Fatal uremia may also occur in a patient whose urine is appar- 
ently normal; and, in cases of chronic contracted kidney, albumin 
may be absent from the urine for long periods of time. The 
temperature of the body may also be used to differentiate between 
uremia and epilepsy. In 1865 Kien called attention to the fact 
that even when uremic convulsions are most violent they are 
accompanied by a fall of temperature of as marked a character 
as the rise noted in epilepsy. Since then this has been con- 
firmed by Roberts, Hirtz, Hutchinson, Charcot, Bourneville, and 
Teinurier. 

The diagnosis between puerperal eclampsia and epilepsy consists 
chiefly in the acuteness of the attack, and the fact that with no 



CONVULSIONS OR GENERAL SPASMS 449 

previous convulsive history a woman becomes suddenly convulsed 
during the pregnant or puerperal state. This is not the place for 
a discussion of the identity of uremia and puerperal eclampsia, 
although uremia is possibly responsible for the nervous disturbance 
in some cases. If the convulsions are uremic, the temperature, 
according to the investigators just quoted, should fall; and accord- 
ing to Bourneville, puerperal convulsions are distinctly separated 
from those of uremia by reason of the fact that the temperature 
rises with great rapidity in the very beginning of the convulsions, 
and there remains with great steadiness. The condition of bodily 
temperature can, therefore, be used to differentiate puerperal 
eclampsia and uremia. 

The separation of syncope from epilepsy is one of the easier tasks 
imposed upon us. The color of the face, the weakened heart beat, 
sudden loss of consciousness, and the general appearance aid us 
here very much, but it is to be recalled that in " Stokes-Adams 
disease" epileptiform seizures are often present. 

Epileptiform convulsions may come on in adults as the result of 
multiple sclerosis, and they are very commonly seen in sunstroke 
when the patient is first attacked. 

Severe convulsions have been known to follow irrigation of the 
pleural cavity after aspiration, and they may also be seen in young 
children suffering from whooping cough at the time of the 
paroxysm. 

Convulsions, which are epileptiform, sometimes occur in the 
later stages of Addison's disease. 

Before closing this portion of this chapter the writer must bring 
forward the points to be used in differentiating epilepsy from those 
attacks simulated by malingerers. Very serious injuries are 
sometimes submitted to by these persons to carry out their designs. 
The points to be looked into are: the condition of the pupils, which, 
in the simulated attack, always react normally; the corneal re- 
flexes cannot be held back; the color of the face is rarely changed; 
and the thumbs are rarely flexed as they should be. Marc has 
pointed out that in malingerers the bystander can readily straighten 
out the thumbs and that they remain so; whereas in epilepsy they 
instantly become flexed again. 

Suggestions as to movements are sometimes followed by malin- 
gerers, and the convulsant movements themselves generally lack 
the bizarre character so typical of epilepsy. 

If amyl nitrite, a lighted sulphur match, or ammonia be held to 
the nose of the fraud, he generally is forced to disclose Lis true 
nature, but these drugs have no effect upon the unconscious 
epileptic. 

The fact that in malingerers there is no rise of temperature 
may also serve as a differential point. 
29 



45° CONVULSIONS OR GENERAL SPASMS 

Convulsions Appearing in Infants or young children may result 
from injuries to the brain in birth, from the presence of growths, 
from the various forms of meningitis, and from irritation of the 
alimentary canal. They also occur in polio-encephalitis. 

There is one variety of infantile convulsive seizure due to 
meningitis, which is often tuberculous and associated with 
retraction of the head and squint; and another variety in which 
the symptoms very closely resemble those due to actual meningeal 
lesions, but in reality is quite independent of them. This con- 
dition has been called "pseudomeningitis." or " hydrocephaloid 
disease," and is seen in young infants generally after attacks of 
severe diarrhea. The fontanelle is depressed, the child is somnolent 
or comatose, and fever may or may not be present. The prognosis 
in the first class of cases is very bad. In the second class it is bad 
enough, but recovery quite often occurs if the treatment generally 
employed in the first class is set aside and a highly nutritious and 
supporting treatment is instituted. 

If a child suddenly develops symptoms of acute meningitis, and 
has delirium, rigidity of the neck, and the major manifestations of 
the disease, the lungs should be carefully examined for croupous 
pneumonia, as this disease in children very often causes these cere- 
bral or meningeal symptoms. Even in the adult maniacal delirium 
and rigidity of the neck may be present in croupous pneumonia, 
owing to meningeal involvement. (For Kernig's Sign, Brudzinski's 
Sign, and the Contralateral Reflex, see chapter on Headache, 

P- 427-) 

Tetanic Convulsions.— The convulsions which are of spinal 
origin, namely, those that are tetanic, are the result of tetanus or 
the ingestion of strychnine in poisonous dose, or its fellow ignatia, 
and sometimes are due to hysteria 

Tetanus convulsions and strychnine poisoning are to be separated 
from one another by the fact that in tetanus the locking of the 
jaws comes first, while in strychnine poisoning it comes last. The 
convulsions of tetanus rarely, if ever, completely relax, while those 
of strychnine do have periods of complete relaxation. There is a 
different history in each case: in one, perhaps, of an injury, as of 
a nail run into the foot; in the other, of a dose of poison having 
been swallowed. Tetanus usually comes on gradually, strychnine 
convulsions suddenly. 

The differential diagnosis between strychnine poisoning and 
hysterical convulsions is more difficult. The convulsions are 
rarely so persistently tonic in hysteria as in strychnine poisoning, 
and the peculiar expression of the hysterical face is often seen in 
this disease. The history of the patient, if obtainable, will throw 
much light on the case and aid very materially in the separation 
of the two conditions. 



TETANIC CONVULSIONS 45 1 

When a patient is seized with sudden and symmetrical tonic 
spasms of the hands, extending to the upper arms and shoulders, 
so that the ringers are flexed at the metacarpophalangeal joints and 
extended in the phalangeal joints, and the lower limb is flexed, 
while the legs are extended and the toes are flexed, the condition 
is one of tetany. (See chapter on the Hands and Arms, "accouch- 
eur's hand.") It is most commonly seen in hysterical cases and 
has no relation to true tetanus. Pressure on a nerve trunk or 
bloodvessel will often produce an attack in such persons, and this 
is sometimes called "Trousseau's symptom." The pressure must 
be applied for several minutes in some cases, and the best place 
to apply it is the bicipital sulcus or the crural sulcus. Sometimes 
pressure on the brachial plexus or on the popliteal space will be 
provocative of an attack. It is not a constant symptom, but 
pathognomonic if found. Another equally useful diagnostic sign 
is called Chvostek's facial symptom. This results from the fact 
that the facial muscles are irritable, so that when they are tapped 
by the finger tip, or a rubber hammer, contraction results. The 
tapping is usually applied over the zygomatic arch in its anterior 
portion, and this will result in a spasm of the upper lid of the eye 
and the alae nasi. In other cases stroking the area over the parotid 
will have the same effect. The muscles in tetany also have an 
increased electrical excitability. (Erb's symptoms.) 

It is worthy of note that both Trousseau's and Chvostek's 
symptoms are sometimes met with in rachitic children, par- 
ticularly if they have craniotabes. (See chapter on the Head.) 
Laryngismus stridulus will often be found associated with tetany 
and rickets. 

Under the name Escherictis pseudotetanus a curious symptom 
conplex characterized by persistent generalized tonic contractions 
of the muscles of the neck, back, legs, and jaw has been described. 
It may occur alone or in association with an acute infection as 
diphtheria. It is not a true tetanus, as its name implies, and is 
really a form of tetany. 

General spasms, in distinction from convulsions, are represented 
by chorea in its various forms, and by saltatoric and palmic spasm, 
paramyoclonus multiplex, and the occupation-neuroses. There 
are other localized spasms from nervous diseases, such as facial 
spasm and wry-neck, athetosis, and posthemiplegic chorea. Some 
of these conditions will be found discussed in the chapter on the 
Hands and Arms and that on the Face and Head. 

When a patient is afflicted more or less constantly and more or 
less universally by disordered, irregular, jerking movements which 
throw the part or parts affected into unusual positions, which are 
not, however, maintained even for a moment, the condition is 
probably chorea minor. Often the speech is seriously disturbed 



452 CONVULSIONS OR GENERAL SPASMS 

by reason of the choreic movements of the lips and tongue or jaws, 
and some loss of power may be manifest in certain muscles. This 
true chorea, or St. Vitus' dance, may affect the whole body or only 
one arm or leg, but generally it is diffused. Commonly it ceases 
at night when the child sleeps, but it often persists day and night, 
and then becomes a serious malady, because of the exhaustion 
produced. It often follows fright, prolonged bad weather, and 
other causes which may upset the nervous balance of the child. 
Chorea in childhood is so characteristic in its manifestations that 
it can be readily recognized in most cases; but it sometimes has 
to be separated in adults from disseminated sclerosis, progressive 
muscular atrophy, hysteria, and Friedreich's ataxia. The move- 
ments in disseminated sclerosis are, however, fine muscular tremors, 
instead of minor jerking movements; and there are present nystag- 
mus and scanning speech in sclerosis, but not in chorea. Again, 
in progressive muscular atrophy there is fibrillary muscular tremor, 
but not twitching of a marked form, and the muscles are wasted. 
In hysteria the muscular movements are rarely choreic, and the 
presence of changes in the color fields and the other stigmas of 
hysteria (see chapters on the Skin and on the Eye) renders a 
diagnosis of the latter condition easy. Friedreich's ataxia is to be 
separated from chorea by its rarity, the scanning speech, scoliosis, 
slow incoordinate movements, and the family history of the disease. 

Rarely when there is some paralysis with chorea, the patient may 
present symptoms of acute poliomyelitis; but the paralysis in the 
latter affection is more marked, and there are no movements in the 
affected muscles, such as occur in chorea. 

Chorea insaniens is a violent form of ordinary chorea associated 
with mania, which is not to be confused with choreic movements 
occurring in the choreic insane. 

Choreic movements sometimes come on in the aged, and must be 
separated from paralysis agitans and senile trembling. This is 
possible by the fact that in paralysis agitans the movements are 
tremors, and there is loss of power with the peculiar facial expression 
("Parkinsonian visage") and a hurrying gait (f estination) . Senile 
trembling is usually an affection limited to the head, and consists 
in a tremor and not in marked twitching. (See chapter on the 
Hands and Arms, part on Tremors.) 

A rare form of chorea has been called Huntingdon's chorea. It 
occurs in adults about the age of thirty to forty years. It is 
hereditary; that is, there is generally a history of the same 
trouble in the ancestors of the patient, and finally as it progresses 
psychical disturbances ensue. Irregular movements first appear in 
the hands, which movements become markedly incoordinated, the 
arms are thrown about in excessive and rapid jerkings, and when 
the infection involves the legs a characteristic gait is developed 



TETANIC CONVULSIONS 453 

of a dancing or "hop, skip, and jump" character. Sometimes, 
early in the malady, the movements can be controlled by the will. 
The face passes through slowly formed grimaces, and the gait may 
be staggering. The speech becomes indistinct, and enunciation 
is not clear. Finally, dementia closes the scene. The movements 
of Huntingdon's chorea are not sudden as in true chorea; it is a 
disease of adult life, and mental disturbance is a prominent symp- 
tom. These facts separate it from ordinary chorea. 

When the patient is involuntarily bends over in a profound bow 
the cause of his movements may be rhythmical contraction of his 
abdominal muscles, producing the so-called salaam convulsions or 
chorea major. 

A still more rare malady is electric chorea or "Dubini's disease," 
in which the muscles of the arm and then the leg on the same side 
are affected with a sudden muscular spasm or shock, such as is 
produced by the electrical current. Wasting of the affected 
muscles, loss of faradic irritability, occasional epileptic convulsions, 
and rarely elevation of temperature come on. The disease is a 
fatal one, and generally occurs in malarial regions in Italy. Under 
the same name of electric chorea Bergeron has described a state 
of rhythmical muscular spasm which usually ends in recovery. 

When a condition of clonic muscular spasm affecting the trunk, 
limbs, and perhaps the neck is present, the hands and toes being 
uninvolved, as a rule, the possibility of the presence of paramyo- 
clonus multiplex is to be considered. The spasms in this rare disease 
are bilateral and occur at intervals, often only on an attempted 
movement or speech. So violent are the muscular contractions in 
some cases that the patient may be thrown to the ground, or, if 
in bed, to the floor. These movements may vary from 3 or 4 to 
120 per minute, but are generally about 50 per minute. The 
symmetrical bilateral involvement, the fact that the movements 
are not choreic in character, and that the patient is a male, are 
to be remembered in making the diagnosis. The ultimate prognosis 
is favorable unless the movements are so constant as to cause 
exhaustion. Care must be taken not to confuse hysterical move- 
ments with this condition. The bilateral movements which affect 
only the larger muscles, and the fact that paramyoclonus multi- 
plex is nearly always seen in the male, separate it in part from 
hysteria, while the hysterical stigmas when they are present will 
point to hysteria as the cause of the disorder. 

Sometimes a patient will be met with in whom, when he 
attempts to stand, the leg muscles first become rigid and then 
are thrown into violent contractions, which cause him to jump 
up and down, or he may be thrown to the floor. This condition 
is called saltatoric spasm, or "jumpers." It is to be separated 
from the condition of the legs seen in lateral sclerosis of the cord 



454 CONVULSIONS OR GENERAL SPASMS 

by the fact that in the latter disease the legs become spastically 
stiff on attempting to use them, from Huntingdon's chorea in that 
voluntary movements with the hands may be performed perfectly, 
and from chorea minor by the absence of small incoordinated 
twitchings. Such a patient will often act on suggestions or in 
imitation of the acts of other persons or of animals. 

Some writers confine the term "saltatoric spasm" to those 
cases which possess no imitative features. In such cases the 
disease is far more moderate in its manifestations. 

Quite distinct from these clonic spasms of the muscles brought 
on by attempted movement is that in which the muscles become 
tonic on attempted movements. At first they are stiff and slow 
in their movements, but ultimately develop a tonic spasm, so 
that walking is at first almost impossible, but the limbs limber 
up on exercise. This is a rare affection, called Thoms.en's disease, 
or one of the forms of myotonia congenita. (See chapter on the 
Feet and Legs.) 

Forced gyratory movements of the body are sometimes seen as 
the result of a lesion of the middle peduncle of the cerebellum. 



CHAPTER XVIII. 

HICCOUGH, VOMITING, REGURGITATION, AND THE 
CHARACTER OF THE VOMIT. 

Due to uremia — Cerebral lesions — Intestinal obstruction — Peritonitis — Cholera 
— Gastric disease — Hepatic disease — Poisons — The appearance of vomit. 

HICCOUGH. 

Hiccough, or singultus, may or may not possess considerable 
clinical significance. Often it arises from slight indigestion. In 
other cases it is produced by the drinking of sparkling wines or 
waters. When hiccough becomes persistent it is a symptom to be 
regarded with interest, for if it continues for a long period of time 
it is usually significant of hysteria or uremia, while if it develops 
in a patient exhausted by some prolonged or severe illness it shows 
deep depression of nervous tone, and is itself dangerous because 
of the exhaustion it speedily produces. Sometimes it is said to 
be an annoying symptom after passing catheters or bougies in 
cases of stricture in the urethra. Hiccough develops in peritonitis, 
and is a most distressing symptom. It is also seen in cases of 
intestinal obstruction and when abdominal growths are developing. 
Singultus also takes place in some cases of cerebral hemorrhage, 
in myelitis affecting the upper parts of the spinal cord, and in 
very rare instances because of severe mediastinopericarditis 
involving the phrenic nerve. It also occurs as a result of central 
nervous irritation in persons suffering from advanced anemia, 
and in cases of suppurative hepatitis. 



VOMITING. 

Vomiting is the act by which the contents of the stomach are 
forcibly expelled from this viscus through the cardiac orifice, the 
esophagus, the pharynx, and the mouth. The vomiting centre 
in the medulla oblongata gives rise to the necessary nervous 
impulses, and is provoked to this by direct stimulation or by reflex 
irritation. Thus in uremia the vomiting sometimes encountered 
is the result of irritation of the centre by some unknown poison. 
When apomorphine is given the centre is also stimulated. Centric 



456 HICCOUGH. VOMITING, REGURGITATION 

vomiting is also caused by the administration of anesthetics, 
notably ether and chloroform. On the other hand, gastric, intes- 
tinal, or other abdominal disorders may refLexly produce very 
persistent emesis, and for these reasons vomiting is of considerable 
diagnostic importance. 

As vomiting is produced by many maladies, it is a symptom 
frequently met with. It occurs with a certain degree of constancy 
as a complication or symptom of uremia, diabetes, apoplexy, 
brain tumor, brain abscess. Meniere's disease, tuberculous menin- 
gitis, hysteria, intestinal obstruction from its various causes, 
gastric and intestinal indigestion, gastritis, gastric ulcer, gastric 
cancer, peritonitis, nephritic colic, hepatic jaundice, hepatic colic, 
in cholera, yellow fever, and a host of other ailments. Sometimes 
the onset of one of the acute infectious diseases of childhood is 
characterized by vomiting. Not infrequently this symptom 
associated with diarrhea masks the presence of the real cause of 
the illness, as in some cases of croupous pneumonia. 

The vomiting of acute gastric catarrh is generally seen in children, 
and is often preceded by great nausea. The contents of the stomach 
are first gotten rid of, then mucus, water, and bile may be ejected, 
and finally exhausting retching ensues if the attack is severe. The 
tongue in such cases is coated and dotted with red spots from the 
enlarged fungiform papillae, and the epigastrium is tender on 
pressure. There may or may not be fever and looseness of the 
bowels. The attack usually follows indiscretions in diet or exposure 
to cold. 

In adults it not infrequently happens that violent retching and 
vomiting develop as a s)"mptom of so-called bilious headache 
usually accompanied by constipation. 

Vomiting is a frequent coincident symptom of headache, because 
in many cases the headache depends for its existence upon a dis- 
ordered stomach or disordered bowels; but it also appears as a 
characteristic symptom of a condition in which the stomach is 
primarily not at fault, namely, in migraine or hemicrania, in which 
in addition to violent pain in the head on one side, we may have 
hemianopsia, scotomas, and sometimes great pallor or flushing of 
the face. (See Pain.) Usually the vomiting follows the pain. 

Vomiting from chronic gastric catarrh is usually a condition met 
with in adults, and when seen in the male is most frequently the 
result of a frequent use of alcoholic beverages to excess. In 
women it often develops from excessive tea drinking associated 
with errors in diet. When due to alcoholism, the vomiting is 
often present only in the morning before or after taking food, and 
then is called the " morning vomiting of drunkards." (See chapter 
on the Tongue.) 

Vomiting due to true gastritis or inflammation of the stomach in 



VOMITING 457 

its deeper layers is very rare, except as a result of the ingestion of an 
irritant poison or hot liquid. 

Perhaps the vomiting occurring in dilatation of the stomach is 
more typical in its character than any other. This act is often a 
prominent symptom of gastric ectasy, the matters vomited being 
often greenish and extremely fetid, and nearly always profuse in 
amount. Examination of the ejecta will generally show food swal- 
lowed days before, owing to the imperfect digestive action of the 
stomach, and this very inability of the stomach to act on the food 
generally gives, for a long period of time, a sense of weight and 
fulness often amounting to pain, and complained of bitterly. There 
is tenderness over the epigastrium on pressure, and the displace- 
ment produced by the palpation often brings on either acid or 
yeasty eructations or even the vomiting already named. Nausea 
preceding the vomiting is by no means common, there being simply 
a gush of foul liquids from the mouth. After such an occurrence 
the vomiting fails to recur for from twenty-four to forty-eight 
hours, or perhaps for a week — i. e., until the viscus becomes over- 
laden once more. The fluids which are given off on eructation 
are exceedingly acrid, nauseous, and bitter. Sometimes they are 
offensive, but more rarely odorless. The reaction of the vomit is 
almost always acid, lactic and butyric being the acids most com- 
monly found, but the normal hydrochloric acid is usually absent. 
Fibres of meat or masses of semidigested and semidecomposed 
food can be seen by the naked eye or under the microscope, and 
sarcinae and many forms of bacteria swarm in the mass. Particular 
search should be made for the yeast fungus Torula cerevisice, the 
presence of which is a certain evidence of active fermentation. 

(For further information in regard to the symptoms of gastric 
dilatation, see chapter on the Abdomen.) 

Vomiting due to gastric dilatation should not at once lead the 
physician into a diagnosis of stenosis of the pylorus from growth or 
constrictions in this part of the stomach, or from innate feebleness 
of the gastric walls, for it may be due to a growth in the abdomen, 
which by pressure occludes the pyloric opening. (See chapter on 
the Abdomen.) 

Sarcinae ventriculi are found not only in the frothy, dirty looking 
vomit of gastric dilatation, but in that of chronic gastric catarrh, 
cancer, and ulcer of the stomach. If iodine or iodide of potassium 
is added to the vomit, the sarcinae become mahogany red or brown, 
and are easily recognized, occurring in squares which are separated 
by dividing lines (Fig. 159). 

Vomiting is frequently seen in hysteria, in neurasthenia, and it 
also comes on in association with gastric crises in locomotor ataxia. 
The vomiting of hysteria is generally characterized by its per- 
sistent character, often lasting for months, and yet the patient 



458 HICCOUGH, VOMITING, REGURGITATION 

often maintains her normal weight to a surprising degree, either 
because the food which is taken is only vomited in small part or 
because she surreptitiously obtains food when her attendants 
do not know it, which she retains. It is generally associated with 
so many of the hysterical stigmas as to be readily diagnosticated. 
The vomiting of neurasthenia is seen in both sexes, and is par- 
ticularly apt to follow any nervous muscular exertion. Thus in 
one case of the writer's, even a short railroad journey taken by an 
overworked man produced attacks of spinal tenderness with 
vomiting which lasted several days. In some neurotic cases the 
vomiting takes place as soon as the food is swallowed. 




Fig. 159. — Sarcinae ventriculi, with starch granules and oil globules, from 
vomited matters. (Otto Funke.) 

The vomiting of pregnancy is usually a morning vomiting, 
though it may persist all through the day. It has no particular 
diagnostic features in itself, save that there are rarely any signs 
of gastric indigestion. The presence of pregnancy, of course, 
makes the diagnosis clear; and in such cases the physician should 
always examine the urine, since a] though the ordinary vomiting 
of pregnancy is a symptom of the first few months, that occurring 
later on may indicate grave renal complications. (See Uremia, 
in chapter on Coma and in Chapter on Convulsions.) 

Vomiting of a nervous type is a common complication of exoph- 
thalmic goitre, and when it occurs sometimes develops into a 
dangerously severe symptom, owing to its constancy, violence, 
and resistance to treatment. Oftentimes serous diarrhea is asso- 
ciated with it, and these two associated symptoms should not 
mislead the physician into a diagnosis of cholera morbus nor of 
jaundice, for icterus often comes on. 

The vomiting of uremia may be one of the earliest manifestations 
of renal disease, and its presence, when persistent in the absence of 
local gastric or other causes, should always lead to an examination 
of the urine, since valuable time may be lost if the patient 
considered to be suffering from some slight indiscretion in diet. 
Its association either as a preceding, concomitant, or consequent 
symptom of coma renders a diagnosis of uremia probable, while 



VOMITING 459 

a history of uremic amaurosis, colliquative diarrhea, and failure 
of the general health will be very important points in reaching a 
decision. No pathognomonic symptoms of uremic vomiting 
exist unless we consider the urinary evidence a symptom, but in 
some cases the vomited matters smell strongly of carbonate of 
ammonium, resulting from the decomposition of the urea which 
has been eliminated from the blood into the stomach by the gastric 
mucous membrane. Uremic vomiting is, therefore, not only due 
to centric irritation by a poison in the blood, but to irritation 
of the stomach by the urea which is excreted into it. Diabetes 
comparatively rarely produces vomiting by the toxemia which it 
causes, but in any case the urinary examination and polyuria 
decide the diagnosis. 

When vomiting results from cerebral hemorrhage, embolism, or 
thrombosis, the focal or hemiplegic symptoms characteristic of 
apoplexy are present. Possibly the vomiting is more indicative 
of hemorrhage than of plugging of the vessel. A sudden attack 
of vomiting in a previously healthy man of advanced years, or 
in one who is young but has a specific history, should raise the 
question as to the possible presence of one of these lesions; provided, 
of course, that ordinary gastric disorder is not present as a cause. 

The vomiting due to cerebral tumor is generally accompanied by 
the characteristic severe and constant headache, vertigo, a slow 
pulse, impaired memory, and sometimes by epileptiform con- 
vulsions. Further than this, the important diagnostic ocular 
symptom called " choked disk" of the optic nerve is to be sought 
for, and if found is of great positive value. Tumor of the brain, 
if near the base, often causes, too, involvement of the various 
cranial nerves. (See chapter on the Eye.) The vomiting of cere- 
bral tumor is independent of taking food, and commonly comes on 
early in the morning, thereby differing from some of the forms 
of vomiting due to gastric disorder. The vomiting arising from 
cerebral abscess has symptoms precisely like those just named, 
so that a differential diagnosis is almost impossible. The history 
of injury or of an infectious process producing a secondary brain 
abscess may point to this cause of the vomiting: the real points of 
difference are that in abscess choked disk is rarely seen, fever is 
commonly present, and the cranial nerves generally escape. When 
purulent meningitis produces vomiting it may be impossible to 
tell whether this symptom is due to it or to an abscess, as the 
purulent collection may be localized. Vomiting sometimes results 
from profound cerebral anemia of an acute type due to hemorrhage, 
in fainting or in chronic anemia, as in chlorosis. Generally, how- 
ever, the symptom is only a constant nausea. The presence of 
great pallor and other evidences of anemia aid in the diagnosis. 
but it must not be forgotten that some severe anemias are accom- 



460 HICCOUGH, VOMITING, REGURGITATION 

panied by febrile movement and by marked choked disk, which 
should not mislead the physician into a diagnosis of cerebral 
tumor. 

When vomiting is due to cerebellar tumor, the diagnosis is aided 
by the presence of vertigo, the peculiar staggering gait, and finally 
by evidences of choked disk, on ophthalmoscopic examination, 
with disordered vision. 

The vomiting of meningitis is quite frequently an early symptom, 
but it also often occurs later in the disease, and is caused by the 
meningeal irritation, and not by any condition of the stomach, 
unless that viscus has been disordered by the unwise use of drugs. 
This form of vomiting can nearly always be separated from that 
due to other causes by the excessively severe headache, chiefly of 
an occipital type; by the pain in the nape of the neck and in the 
spine; by the rigidity of the dorsal muscles, so that opisthotonos 
may be caused in severe cases; and, finally, by the disordered 
functions of the cranial nerves, as a result of which there are found 
trouble in the oculomotor nerve, strabismus, double or single 
ptosis, slowly reacting pupils, which may be unequal, nystagmus, 
and sometimes facial contractions due to involvement of the facial 
nerve. 

Vomiting due to acute miliary tuberculosis often comes on at the 
very onset of the malady, and is associated with obstinate con- 
stipation, or, on the other hand, active diarrhea; but the fever, the 
very rapid pulse, the wasting of the patient, the possibly present 
physical signs of tuberculosis of the lungs, and, very important, 
the peculiarly severe dyspnea, for which no adequate cause can be 
discovered on physical examination, all point to the general infec- 
tion. If a skilful examination of the eye can be made with the 
ophthalmoscope, the choroid may be found to be studded with 
tubercles. 

The reflex forms of vomiting are very numerous, and depend 
chiefly upon organic and functional disorders of the abdominal 
viscera. In some of these conditions vomiting is of little impor- 
tance, except for its gravity if the patient is exhausted; in other 
words, it is simply a disagreeable symptom. In others the symp- 
tom vomiting is of considerable diagnostic value as indicating 
the grave mischief which produces it. One of the most important 
of the latter conditions is intestinal obstruction, whether it arises 
from intussusception, constrictions by bands, volvulus, or impac- 
tion. 

In intussusception vomiting is practically a constant symptom, 
occurring with the sudden pain, or, at times, even preceding it. 
In children it continues until shortly before death, and is rarely 
feculent. 

In the adult, and in the chronic form, there may be complete 



VOMITING - 461 

absence of vomiting, though this is certainly exceedingly rare. 
Leichtenstern takes exception to the statement that the seat of 
obstruction is indicated by the period at which vomiting is 
developed. The ileum invagination is most frequently accompanied 
by early vomiting, not because of its seat, which is usually but 
little removed from the ileocecal valve, but because it is commonly 
obstructive. The vomiting, both in time of development and in 
nature, will depend not upon the seat of the trouble, but upon 
the presence or completeness of obstruction, and may be early 
if the obstruction is absolute in the sigmoid flexure, and feculent if 
the occlusion is in the upper part of the ileum. 

The pain is usually sudden, violent, diffuse, or, if localized, 
usually centred in the ileocecal or umbilical region. After a few 
hours in children, a much longer interval in the adult, the pain 
ceases, often as suddenly as it commenced, and there is an interval 
in which there is little to suggest that the pathological condition 
still continues. This is followed by a return of the pain, the 
paroxysms becoming more violent and prolonged, the intervals 
less marked as the disease progresses, or in the adult, if the ob- 
struction passes into the chronic form, intervals even of many 
hours may elapse between the paroxysms. The pain is frequently 
accompanied by tenderness, but this is an exceedingly variable 
symptom, and at times pressure seems to relieve the pain. 

Blood-stained mucous evacuation are a symptom of intestinal 
obstruction which, in children, is rarely wanting. It occurs within 
a few hours of the first attack. At the first the discharge is of 
blood-stained feces; later, if obstruction is developed, of blood 
and mucus, and is usually exceedingly offensive. In children 
diarrhea is common throughout the whole course of the case. 
At times, following complete constipation and feculent vomiting, 
there will suddenly appear copious evacuations from the bowel, 
mingled with blood, in which may be found evidences of the 
necrosed intussusceptum. Where this slough is extensive it may 
be lodged in a lower portion of the bowel and cause fatal obstruc- 
tion. 1 

In connection with the mucosanguinolent evacuations, the 
tenesmus or straining is a symptom so common that it is of some 
diagnostic import. That it is not dependent upon the character 
of the evacuation is shown by the fact that it is present in cases 
of complete obstruction. Brinton has shown that this symptom 
is seldom developed except in the ileocecal and colon invaginations. 

A much rarer condition, and one which Leichtenstern ascribes 
to the secondary effect of intense tenesmus, is a patulous condition 

1 For much information on the subject of intestinal obstruction, see the Fiske 
Fund Prize Essay of the Rhode Island Medical Society for 1899, by Dr, Edward 
Martin and the author. 



462 HICCOUGH, VOMITING, REGURGITATION 

of the anus due to paralysis and dependent upon invagination of 
the descending colon and rectum. This is never produced by 
invagination of the i]eum. 

Leich tens tern's statistics show that a tumor can be felt either 
through the parietes or by rectal examination in 52 per cent, of all 
cases. In the first year of life this most important diagnostic sign 
was present in 63 per cent. The tumor is usually felt in the left 
iliac region, or by the finger passed into the anus. The ileocecal 
invagination is most frequently accompanied by demonstrable 
tumor; the ileum invagination exhibits this symptom with less 
frequency. 

Many authors have noted that the tumor varies in size and 
consistency from time to time, now, during an acute paroxysm 
of pain, being hard, knotty, and plainly perceptible, shortly after- 
ward eluding the most careful search. Duchaussoy has described 
two distinct movements which can often be perceived in the 
tumor, namely, the erectile and the vermicular motion. 

Distention of the abdomen is not of great significance, because 
it is often absent. In children especially it may not appear at 
all, or may appear only just before death. In adults, in whom 
obstruction is more common, it may become as well marked as 
in obstruction from any other cause. 

In the chronic form of invagination the symptoms are less violent 
in onset; there may be nothing more characteristic of the attack 
than recurring paroxysms of pain, meteorism, and obstruction, 
with symptoms of intestinal stricture constantly manifesting them- 
selves. These cases terminate either in cure by reduction or by 
extrusion of a slough, or perish from exhaustion, inanition, or in 
the course of an acute attack. 

The additional symptoms upon which a diagnosis of vomiting 
from intussusception is to be based are the acute onset of colicky 
pain, and its intermittent character; passages from the bowels 
containing blood and mucus; the presence of tumor, commonly 
in the left iliac region, or felt through the anus, varying in size 
and consistency from time to time, with an erectile or vermiform 
motion; and the ordinary obstruction symptoms. The diagnosis 
is further confirmed if there are present violent peristalsis and 
tenesmus, and if these symptoms occur in an infant. 

According to Leichtenstern, Bryant, and others, 40 per cent, of 
all cases of intestinal obstruction are due to intussusception, and 
this condition is most common in the first year of life, after which 
it becomes more and more rare until the fortieth or fiftieth year, 
when it increases in frequency. 

Internal strangulation by bands occurs in from 25 to 30 per cent, 
of the cases of obstruction of the intestine, and affects males most 
commonly between twenty and forty years of age. In 133 out of 



VOMITING 463 

151 cases the small intestine was involved. The typical symptoms 
are as follows: 

1. Sudden, agonizing pain, constant, and located about the 
umbilicus, with paroxysmal increments. 

2. A rapid, weak pulse, and subnormal temperature: This is 
nearly constant in the early stages of the attack; later on, when 
local or general peritonitis develops, the temperature and pulse 
may assume the features characteristic of inflammation. 

3. Vomiting: First of the contents of the stomach, then of bile, 
and, finally, in a large percentage of cases, of feculent matter. 
The feculent vomiting rarely appears before the third day, and in 
cases running a very acute course, death may ensue before this 
symptom has time to develop. The vomiting is constant and 
gives no relief to the patient. 

4. Constipation: Exceptionally there may be one or two 
passages representing the contents of the bowel below the seat of 
obstruction; after that the constipation is absolute, not even flatus 
passing by the anus. Treves has suggested that the evacuations 
sometimes observed toward the termination of the case, and not 
due to the relief of obstruction, may be dependent upon the begin- 
ning of peritonitis. 

5. Tympanitic distention: Where there is a large segment of 
gut involved in the strangulation its early distention may give 
rise to a localized abdominal enlargement, which is exceedingly 
suggestive as to the cause of the attack. In general, the meteorism 
is not marked except when peritonitis supervenes. 

Since in the large majority of cases the obstruction is localized 
in the lower portion of the small intestine, the primary disten- 
tion will be observed in the middle abdominal region— i. e., the 
epigastric, umbilical, and hypogastric areas. Laugier claims by 
this symptom to locate the obstruction with some certainty. 

The violent peristalsis and repeated vomiting prevent the 
extreme meteorism characteristic of intestinal paralysis. 

6. Localized tenderness and percussion dulness: When present 
these signs are of exceedingly great importance, since they denote 
the position of the strangulated bowel. 

Exceptionally a tumor may be felt, formed by the congested gut 
or the matting together of the intestinal coils. 

The urine is diminished in quantity and may be suppressed. In 
acute strangulation it commonly contains albumin, and it is 
stated that this is of diagnostic value. 

In this connection the history is of great importance. 

Other congenital deformities would suggest the possibility of 
Meckel's diverticulum as a cause. 

A preceding typhlitis, pelvic peritonitis, or severe abdominal 
traumatism would respectively assign an adherent vermiform 



464 HICCOUGH, VOMITING, REGURGITATION 

appendix, peritoneal bands, or rents in the omentum or mesentery 
as the causative agents in the production of the symptoms. 

The age of the patient should also be considered, since this form 
of obstruction usually occurs between the twentieth and fortieth 
years. 

The sudden onset of violent, persistent pain, subnormal temper- 
ature, and frequent pulse, the obstinate, absolute constipation, the 
persistent, repeated vomiting, becoming fecal, and the rapid 
course of the disease, all point to internal strangulation. 

Auscultation of the abdomen is at times of value, a sound 
compared to the click of the water-hammer being heard most 
distinctly at the point of obstruction. 

Palpation and percussion should not be omitted, as thereby the 
seat of obstruction has been distinctly located. 

Volvulus is the most frequent form of intestinal obstruction after 
intussusception and that due to strangulation. Vomiting occurs, 
but is not so constant a symptom as in those forms first named. 
Thus it occurred in from 8 per cent, in Brin ton's statistics to 2.5 
per cent, in those of Treves, and 4 per cent, in Martin's and the 
author's. It is nearly always seen in men in middle life. The 
vomiting is rarely fecal, is very slight in many cases, and sometimes 
does not appear at all. 

Vomiting, on the other hand, is quite commonly seen in the 
cases of obstruction from impaction or obstruction from foreign 
bodies. The distention is slight, the amount of systemic shock 
far less than in other forms of obstruction, and the duration of 
the attack somewhat longer than usually obtains in this class of 
affections. The symptoms of obstruction are frequently only 
partial, the vomiting being moderate in amount and not ster- 
coraceous, the constipation not being absolute. 

Except in the case of enteroliths and very large foreign bodies 
a tumor can rarely be felt. 

It is often impossible to diagnosticate this form of obstruction 
from that depending upon a narrowing of the lumen of the bowel, 
such as is produced by cancer or stricture. The previous history 
is always of great importance. 

In this connection it is to be remembered that hemorrhagic 
infarction of the intestine may produce symptoms similar to those 
just described, namely, pain in the region of the navel, or more 
generally throughout the belly, fecal vomiting, diarrhea, and 
bloody stools. Actual obstruction may be present. Search should 
be made for a source from which an embolus may arise, as, for 
example, valvular cardiac disease, and if this is found the likelihood 
of infarction being present is increased. 

When persistent vomiting develops in an infant during the first 
few weeks of life and no error in diet can account for the symptom, 



VOMITING 465 

the physician should consider the possibility of the presence of 
congenital hypertrophic stenosis of the pylorus. At first the sym- 
tom may be present only after food is taken and the quantity 
ejected may be small or it may be greater in amount than the food 
recently swallowed, indicating retention in the stomach of a 
former meal. Bile is never present in the vomit. In a few days 
the stomach becomes remarkably intolerant of food and the 
vomiting may be projectile in character. Rapid emaciation takes 
place and the physician may on palpation find a tumor at the 
pylorus. On inspection waves of contraction in the walls of the 
stomach may be seen passing from left to right. 

When vomiting arises from general peritonitis it is often one of 
the earliest symptoms of the malady. It is almost always present, 
and is often a very severe symptom, and associated with or is 
replaced by a constant retching, which adds to the exhaustion of 
the patient. At first it may only follow the swallowing of food, 
but often it occurs without such a cause, and after the stomach is 
emptied of its ordinary contents glairy, watery mucus is expelled, 
which is often of a distinct greenish tint. The great tenderness of 
the belly in acute peritonitis, the moderate fever, the rapid pulse, 
the anxious face, and the cold skin as collapse approaches, all 
render the diagnosis easy; but it is to be remembered that the 
distention of the belly by an overfilled bladder or pregnant uterus 
may mislead the physician into thinking that peritonitis is present 
because of the swelling, the pain, and the vomiting. Vomiting 
is not a severe symptom of appendicitis unless the peritoneum has 
become involved in the inflammatory process, although it may 
occur once or twice when the pain in the appendix is most severe. 
The localization of the symptoms in the neighborhood of the 
appendix makes the diagnosis possible. (See chapter on the 
Abdomen.) 

When vomiting occurs in typhoid fever it is usually a symptom of 
bad feeding or imperfect digestion, and is rarely of grave importance 
except under two conditions. The first of these is when it occurs 
as a result and symptom of intestinal perforation, an accident 
commonly seen late in the disease; and, second, when it takes place 
as an obstinate and exhausting symptom after the fever has 
practically passed by, from unknown causes, probably toxic in 
character. The symptoms of perforation other than vomiting 
can be found in the chapter on the Abdomen and Abdominal 
Viscera. 

Vomiting as a symptom of cholera is accompanied by serous 
diarrhea of profuse character, by the development of collapse. 
cramps in the muscles, anuria, and great circulatory failure. It 
should be separated from the vomiting due to cholera morbus or 
severe indigestion, antimonial poisoning, and arsenical poisoning. 
30 



466 HICCOUGH, VOMITING, REGURGITATION 

Cholera morbus is to be separated from cholera, first, by the 
absence of the comma bacillus in the stools; second, by the fact 
that there is a history of exposure to cold or damp, or bad food; 
third, by the absence of an epidemic; and fourth, by the fact that 
its manifestations are milder. 

No one can be skilled enough to separate symptoms of poisoning 
by antimony from those due to cholera, for they are identical in 
every way. Nothing but the history of the ingestion of the poison 
and the discovery of antimony in the excretions can prove the 
case to be one of antimonial poisoning, particularly if an epidemic 
of cholera is present. 

In arsenical poisoning the association of vomiting with bloody 
stools separates the symptoms from those of cholera. 

Vomiting is often a very severe and early symptom of cholera 
infantum (see chapters on the Abdomen and on Bowels and Feces), 
and it occurs in attacks of true dysentery as, a common symptom, 
when its underlying cause is readily discovered. (See Abdomen.) 

The diseases of the stomach causing vomiting are cancer, ulcer, 
gastritis, catarrh (acute and chronic), true gastritis, and dilatation. 

The vomiting of gastric cancer at first consists in the expulsion 
from the stomach of its contents — mixed particles of food, mucus, 
water, and sometimes bile. The vomit may be tasteless or sour 
from fermentation, and may have an offensive odor from similar 
causes. Often it contains blood, either in bright-red streaks or as 
a brownish-red fluid, or in similarly colored clots, which may be 
brown when they have been in the stomach for some time. Often 
the exuded blood, changed by mixing with the stomach content, 
looks like coffee grounds, producing "coffee-ground vomit." This 
coffee-ground vomit is not pathognomonic of gastric cancer, but 
is very characteristic of this disease. (For the other symptoms 
of gastric cancer, see chapter on the Abdomen.) 

Vomiting due to gastric ulcer is preceded by pain, and is generally 
brought on by taking food, and so occurs soon after eating. The 
food is, therefore, only slightly digested, and evidences of fermenta- 
tion are absent to a great extent. If blood is present, it is nearly 
always bright red and in considerable quantity, and indicates 
that a hemorrhage has recently taken place from the surface of an 
ulcer. Very profuse hemorrhages into the stomach may cause 
vomiting by irritating and distending this viscus. The history 
of vomiting after eating, the presence of blood in the vomit, the 
pain in the stomach, the age of the patient (generally twenty to 
thirty years), the sex (generally female), and the hyperchloric 
acidity, combined with the other symptoms (see chapter on the 
abdomen), complete the diagnostic array of facts. 

There are, however, other causes of vomiting of blood or hema- 
temesis than gastric ulcer and cancer. Thus, it occurs from 



VOMITING 467 

obstruction to the portal circulation from hepatic cirrhosis, and 
from growths and splenic affections which result in varicosity of 
the bloodvessels of the stomach. Hematemesis also follows severe 
blows, kicks, and other injuries to the epigastrium. Sometimes 
it takes place in cases of heart disease in which there has resulted 
hepatic engorgement with secondary gastric congestion, and it may 
be developed in small degree by any form of violent vomiting 
which strains the stomach, particularly if an irritant substance 
has already destroyed the mucous membrane. Again, hematemesis 
is seen in scurvy, typhus, yellow fever, and acute yellow atrophy of 
the liver, as a result of breaking down or destruction of the coats 
of the vessels. Sometimes it is seen in cases of dengue, in influenza 
of the epidemic type, and in relapsing fever. Hematemesis may 
also occur in purpura hemorrhagica, in hemophilia, and possibly 
as vicarious menstruation. In malarial fever of a severe character 
the dark-colored vomit is generally due to bile, but it may be due 
to exuded blood. Such a case is reported by Boon as occurring 
in a child. 

Coffee-ground vomit is also sometimes seen in cases of locomotor 
ataxia following a gastric crisis. Roux asserts that overdoses of 
iodide of potassium may produce a gastric crisis in locomotor 
ataxia by irritating the stomach. 

Care should always be taken that the physician is not misled by 
the vomiting of swallowed blood into a diagnosis of gastric hemor- 
rhage from any of the causes just named. It may enter into the 
stomach from the pharynx, as after epistaxis, or blood may be 
swallowed by a malingerer. Hematemesis is to be separated from 
hemoptysis by the fact that in the latter there are physical signs 
in the lungs, the sputum is frothy and bloody, there is absence of 
retching or vomiting movements, and the blood is brighter red 
in hemoptysis than in hematemesis, as a rule. 

Under the name of melena neonatorum there is a condition of 
hematemesis occurring in children within the first few days or 
weeks of life. This condition has been thought by Leube to be 
due to gastric and duodenal ulcers, and his views are indorsed by 
Buhl and Huhn, Spiegelberg, Binz, and Landau. In one of the 
latter's cases thrombosis of the umbilical vein was present, and it 
has been thought that when expansion of the chest takes place 
in the newborn child small clots may escape from this vessel through 
the ductus arteriosus into the descending aorta and gastric arteries, 
and thus cause an ulcer of the stomach by embolism. 

Cyclical vomiting already mentioned is generally seen in children, 
and is of rare occurrence. It is characterized by attacks of vomiting 
recurring after intervals of uncertain length, during which the 
patient may seem entirely well. The attack may last from a few 
hours to a few days. There are often pain in the epigastrium and 



468 HICCOUGH, VOMITING, REGURGITATION 

constipation. Sometimes retching is the main symptom. It is 
generally seen in children more rarely in neurotic adults, and is 
probably a form of acid intoxication. 

In acute pancreatitis there is colicky pain in the epigastrium, 
deeply seated and extending to the right shoulder and back, and 
great restlessness, precordial distress, dyspnea, and faintness are 
present. The matters vomited are greenish, clear, and viscid, 
and the efforts at vomiting increase the pain. There is no jaundice, 
but death soon comes to the relief of the patient. 

As an early diagnosis of acute pancreatitis may permit surgical 
interference, with possible recovery of the patient, the diagnosis is 
important. The mistake commonly made is to consider the case 
one of intestinal obstruction. 

Vomiting of a peculiar character is always present in phosphorus 
poisoning. The symptoms associated with ingestion of the poison 
may not come on for some hours. At the end of that time the 
peculiar taste of phosphorus may be noticed in the mouth, the 
breath is heavily laden with its odor, and burning pain in the 
esophagus, stomach, and abdomen ensues. Vomiting and purging 
now assert themselves, and the matters vomited and those passed 
from the bowels may be luminous in the dark, owing to the presence 
of free phosphorus. The vomit is at first made up of food, then 
mucus, then bile, then perhaps blood. All the symptoms of a mild 
gastro-enteritis may develop, but it is to be noted that constipation 
of an abstinate type may replace the purging. Very soon the 
liver increases in size, and gives rise to general hypochondriac 
pain and tenderness, as well as local swelling. At the end of 
twenty-four hours, or perhaps after the second day, a cessation 
in the symptoms occurs, and, if the physician be not on his guard, 
this will lead him to a hopeful prognosis. In the course of a few 
hours jaundice begins in the conjunctiva and then extends over 
the entire body. With the onset of jaundice the vomiting and 
pain return with renewed vigor. The matters vomited are often 
the color of "coffee-grounds," due to exuded and altered blood. 
The bowels are absolutely confined, or the few hard masses passed 
are white and clay-like, because of the absence of biliary coloring 
matter. There is no bile in the vomit in this stage, because the 
hepatic ducts have been closed by the inflammation set up in the 
liver. After this nervous symptoms ensue. Muscular twitchings, 
headache, vertigo, wild delirium, erotic convulsions, and, finally, 
unconsciousness and death occur. Sometimes the convulsions 
occur just before dissolution. Even if the patient survive the 
acute stage, he generally dies of the changes produced in his vital 
organs, which consist in widespread fatty degeneration, even in 
the acute stages. Atrophy of the liver, destruction of the gastric 
tubules, pancreatic involvement, and kidney degenerations aid 
in producing the ultimately fatal result. 



VOMITING 469 

The symptoms may so closely resemble those of acute yellow 
atrophy of the liver as to make a differential diagnosis impos- 
sible, unless some evidence of the presence of phosphorus is 
obtainable. 

Meniere's disease is associated with vomiting, the contents of the 
stomach being expelled after the attack of vertigo and tinnitus 
aurium. 

The affections of the liver which sometimes result in vomiting 
are chiefly atrophic cirrhosis which results in gastric catarrh, in 
time causing the morning vomiting of drunkards, catarrhal 
and obstructive jaundice, hepatitis, hepatic abscess, and pyle- 
phlebitis. The rapid development of jaundice, hepatic tenderness, 
and swelling, or a history of violent hepatic pain (colic), renders 
the diagnosis possible in the case of jaundice. (See chapter on 
the Skin.) Hepatitis — that is, hepatic abscess — is often accom- 
panied by or produces vomiting which is apt to be very obstinate. 
The swelling of the liver, the tenderness in the hypochondrium 
on palpation, the pain in the hepatic region, often referred to the 
neighborhood of the right shoulder, and the febrile movement, 
which is intermittent, sweeping up to 104 or 105 °, then down to 
normal, are the chief characteristic symptoms. (See chapter on 
the Abdomen.) Vomiting accompanied by a similar train of 
symptoms also occurs in cases suffering from pylephlebitis. 

Violent vomiting associated with great pain in the loin, radiating 
down into the testicle, or inside of the thigh, indicates the pres- 
ence of a renal calculus, either in the pelvis of the kidney or in 
the ureter. 

Hemoglobinuria is sometimes accompanied by vomiting. The 
attacks are paroxysmal, and are often ushered in by persistent 
yawning, with pain in the limbs, headache, nausea, and vomiting, 
followed by moderate fever, which is preceded or accompanied by 
a chill. Pain may be felt in the liver, but, more pathognomonic 
than all, the urine is soon found to be dark, brownish red, or even 
black, owing to the presence in it of hemoglobin. 

When vomiting occurs in yellow fever , the presence of an epidemic, 
the suffusion of the eyes, the headache, the black character of the 
vomit, the slow pulse, scanty urine, and prostration, all point to 
the cause of the symptom. 

Vomiting is a frequent symptom in some cases of phthisis, 
particularly if laryngeal tuberculosis is present. It also occurs as 
a result of swallowing the sputum instead of expectorating it, 
and very commonly excessive cough produces vomiting, especially 
if the cough follows closely after a meal. 

Closely associated with the vomiting due to these causes is that 
occurring in cases of pulmonary gangrene. 

In children suffering from whooping cough vomiting often take^ 



470 HICCOUGH, VOMITING, REGURGITATION 

place at the close of the paroxysm, and is due to the spasmodic 
movements of the chest and diaphragm. 

Finally, it is not to be forgotten that vomiting often ushers in 
any one of the eruptive diseases, such as the fevers, syphilis in its 
early secondary stages, and erysipelas. 

Under the name of merycismus cases of voluntary regurgitation 
of food have been reported, chiefly outside of the United States. 
The patients have been nervous or hysterical persons. 

The Vomit. — Aside from the diagnostic significance of the act 
of vomiting, the physician should remember that the vomit itself 
may give him information as to the condition of his patient. 

Under the head of gastric dilatation I have spoken of the 
significance of vomiting large amounts of liquid and undigested 
food, so that it is not necessary to speak of this point here; but it 
is well to remember that small amounts of vomited material often 
possess considerable diagnostic importance. In the severe retching 
of cerebral disease or uremia very little material is gotten rid of, 
and in uremia this may be ammoniacal. In cases in which small 
quantities of exceedingly sour, clear liquid are vomited, we often 
find that the attack is due to migraine or nervous headache. If 
watery liquid and mucus are vomited, there is probably gastric 
catarrh. The vomiting of bile is usually only seen when repeated 
retching has drawn this secretion into the stomach. The liquid 
may be either golden yellow or greenish in hue. Somewhat like 
this vomit is that seen in peritonitis, in which disease grass-green 
material is often expelled. Similar material is also vomited in cases 
of intestinal obstruction before stercoraceous vomiting comes on. 

The vomit of intestinal obstruction is sometimes fecal in odor 
for obvious reasons. If odorous poisons have been taken, the 
vomit smells of the poison; and if there be phosphorus present, 
the vomit not only smells of it, but in addition may be luminous 
in the dark. 



CHAPTER XIX. 
COUGH AND EXPECTORATION. 

The varieties of and diagnostic significance of cough — The causes of cough — 
The sputum — Its pathological significance. 

The significance of cough as a symptom is very important, and, 
though it may arise from many causes, in the majority of instances 
it points to disease in the chest, in the trachea or the larynx, in the 
pharynx or in the nose. Rarely it is a purely nervous trick, and 
equally rarely it arises from irritation in the stomach (" stomach 
cough," so called). A cough is said to be dry and hacking when it 
fails to bring up into the throat or mouth any secretion, or when 
it is short and sharp. Often such a cough is paroxysmal; in other 
cases it consists in single but fairly frequently repeated, short, and 
forcible expiratory efforts, as if the patient was trying to clear his 
throat. A loose cough is nearly always paroxysmal; that is, it 
occurs "in spells," and at nearly every paroxysm results in the 
raising of some mucus. The first variety of cough is that seen in 
the early stages of phthisis pulmonalis, acute bronchitis, or pneu- 
monia, before any exudation has taken place ; in the early part of a 
paroxysm of asthma; in the early portion of an attack of whooping 
cough and when the cough arises from irritation in the upper 
air passages, whether this be due to the inhalation of dust or the 
presence of some growth, as a laryngeal papilloma. The loose 
variety of cough is seen in the later stages of acute bronchitis, 
pneumonia, asthma, whooping cough, and in cases of emphysema 
with bronchiectasis, and in the stage of pulmonary tuberculosis 
associated with the breaking down of lung tissue, the formation 
of cavity, and the development of bronchitis with it, and in 
gangrene of the lung. 

There are two peculiar forms of cough to be mentioned, namely, 
the so-called barking, brassy, ringing laryngeal cough, which we hear 
most typically in false or spasmodic croup, and the cough of whooping 
cough, which is, as its name implies, the most typical which we meet 
with. Suddenly the child begins to give a series of quick, sharp 
coughs, which become more and more rapid until the chest is 
nearly emptied of air. In the early stages of the disease this is all 
that occurs, and unimpeded inspiration ensues; but later the cough 
no sooner ceases from exhaustion of the lungs of air than with 
the attempt at deep inspiration the glottis closes spasmodically. 



47 2 COUGH AND EXPECTORATION 

and the air is sucked throught the chink with a whooping sound. 
The flushed or cyanotic face of the child, associated with these 
paroxysmal attacks, renders the diagnosis easy. 

There is nothing distinctive in the cough of early stages of 
pulmonary inflammation, whether it be bronchial or vesicular, 
although, if the bronchitis be very intense or if the pulmonary 
inflammation also affect the pleura, the cough may be partly 
smothered or suppressed by the patient, who endeavors to control 
or stop it in order to escape the pain it causes. To this end he 
sits or lies in bed, endeavors to fix the muscles of his chest so that 
they will not respond to the reflex cough impulse, and shuts his 
lips or holds his breath, although very often the reflex irritation 
overcomes his will-power and the cough bursts through his com- 
pressed lips with an expression of pain. Such a suppressed cough 
is always indicative of pain. 

In all forms of dry cough there is now and again a small plug of 
mucus expelled from some part of the respiratory mucous mem- 
brane. Such coughs possess no value to the patient, being merely a 
sign of reflex irritation; but a loose cough, unless it is very excessive, 
is of the greatest possible use to the patient, for it is an effort on the 
part of nature to rid the lungs of abnormal exudations or secretions. 
For this reason this symptom is not to be removed completely in 
cases of resolving pneumonia, pulmonary tuberculosis, or bronchi- 
ectasis with excessive secretion, since if drugs are given which stop 
the cough, the lungs are speedily filled with the secretion; and in the 
case of tuberculosis, or gangrene, or mucopurulent bronchitis, septic 
absorption results. Similar good results are reached by the cough 
of pulmonary abscess, and when an empyema has broken into a 
bronchial tube. 

When the patient complains of chronic cough, which is worse 
in, or confined entirely to, the morning hours, and tells us that 
the cough finally causes the discharge of much secretion, and that 
this is followed by freedom from cough for many hours, the case 
may be one of tuberculosis with cavity, pulmonary abscess, empyema 
which has ruptured into a bronchus, or sacculated bronchiectasis. 
Such coughs come on in paroxysms whenever the lung must be 
relieved, and the length of the paroxysm depends upon the looseness 
of the secretion and its situation in the lung. Thus, if the secretion 
be in the larger bronchial tubes, it is easily expelled; whereas if 
it be in smaller bronchi, or at the bottom of a cavity, great and 
frequently repeated effort will be required before the liquid can 
be raised into the mouth for expectoration. 

The presence of an obstinate cough due to bronchitis, which 
resists all ordinary treatment, should lead the physician strongly to 
suspect that one of three ailments is present, namely, undiscovered 
tuberculosis, cardiac failure, or Bright's disease. 



COUGH AND EXPECTORATION 473 

The cough of acute laryngitis may be quite severe, and occurs 
in short, sharp barks of a harsh or brassy character (like spasmodic 
croup) , which is so typical as to be called a laryngeal cough. The 
association with this cough of partial or complete ]oss of voice and 
pain in the larynx, with a history of exposure to cold and dust, or 
of the excessive use of the larynx in speech or singing, renders the 
diagnosis clear, even if the laryngoscope is not used to discover 
congestion and inflammation of the laryngeal mucous membrane. 
In the false croup of children, which is always associated with 
laryngeal irritation, the barking, ringing cough is so characteristic 
as to render a diagnosis possible as soon as the sound is heard, 
and with it there is dyspnea due to obstruction to breathing. 

The cough of the laryngeal phthisis is not so typically brassy and 
ringing as that of acute laryngitis, but the presence of pain in the 
larynx, hoarseness, and persistent laryngeal dryness should lead 
to a search for tuberculosis by the laryngoscope, and an examina- 
tion of the chest for physical signs of trouble in the lungs and of 
the sputum for tubercle bacilli. 

Sometimes cough of a laryngeal character is due to an aneurysm 
pressing upon the larynx. In other cases the cough depends not 
upon the pressure of an aneurysm, but upon the pressure produced 
by carcinoma of the esophagus or by a mediastinal tumor. 

Cough due to the inhalation of irritant dusts or vapors is often 
present is girls who work in carpet factories, in the air of which 
there are immense quantities of fine particles of wool. Again, it is 
seen in knife-grinders, needle-workers, coal-miners, and in workers 
in arsenical and lead pigments. 

Sometimes in paralysis of the pharyngeal muscles (glossolabio- 
pharyngeal paralysis) cough is produced by the slow passage of 
food, which may in fact enter the larynx. 

A night or evening cough is very commonly seen in cases of 
respiratory catarrh or more grave disease. It is often absent all 
day, only to return in the evening in cases of laryngitis and in 
phthisis; and in those cases in which it follows getting into bed, 
it is due to chilling of the skin by the cold sheets, which results in 
congestion of the inflamed mucous membrane. 

Quite frequently children suffering from chronically enlarged 
tonsils suffer from cough on going to sleep, especially if the uvula is 
relaxed or elongated. The cause of this cough is that in the relaxa- 
tion of sleep the tonsils touch one another or tickle the uvula. 
As soon as the child wakes muscular contraction separates the 
approximating surfaces and the cough soon ceases. If this cause 
of cough cannot be eliminated we must look further for its origin. 
Not infrequently hypertrophy of the mucous membrane over the 
turbinated bones, so that it presses on the nasal septum, may 
cause cough, and irritation of the inferior and middle turbinated 



474 COUGH AND EXPECTORATION 

bodies and the septum opposite the inferior turbinated body may 
cause reflex cough. So, too, enlargement of the pharyngeal tonsil 
may cause this symptom, as may also elongation of the uvula. 
When chronic enlargement of the tonsils, with follicular accumula- 
tions, is present, cough frequently results. 

The cessation of cough in advanced phthisis, suffocative bron- 
chitis, or the bronchorrhea with bronchiectasis of old persons, or 
in severe pneumonia, indicates exhaustion, collapse, or approaching 
unconsciousness, and is a bad sign. 



THE SPUTUM. 

Macroscopic Examination. — A careful examination of the mate- 
rials expectorated by the patient, or, in other words, of the sputum, 
is of the utmost importance in all cases of disease of the respira- 
tory tract, whether the abnormal process be primary or secondary. 
Sputum varies greatly in its general character on ordinary examina- 
tion, sometimes being very fluid and even watery in consistency, 
and sometimes thick or tenacious. In some instances it is clear 
and glairy-looking, resembling somewhat slightly beaten white of 
egg; in others it is yellow and opaque. Placed on a clean linen 
cloth, the sputum may evaporate to almost nothing, or leave a 
heavy mucopurulent deposit after all moisture is gone. 

The naked-eye appearances of sputum are quite characteristic 
in several conditions. Thus, in the later stages of acute bronchitis 
the sputum is apt to be thick and yellowish, and to contain lumps 
of half -inspissated mucus. In croupous pneumonia it is rusty in 
color, is peculiarly free from watery ingredients, and is gelatinous 
to such an extent that it adheres to the spit-cup, so that when this 
vessel is well filled its contents do not readily fall out even when 
the cup is tipped upside down. The sputum is less red and grayish 
in hue and less adhesive after resolution is well advanced. The 
brightness of the blood in the sputum in cases of pneumonia is 
also a guide to prognosis. Thus, Sir William Jenner said: "The 
less the weight for a given height, the more red blood in the sputum, 
the better the chance for the patient." A dark prune-juice sputum 
in the early stages of pneumonia is on the contrary rather a grave 
sign. 

In pulmonary hemorrhage or hemoptysis, after having, perhaps 
for a short time, a salty taste in the mouth, the patient suddenly 
brings up, with or without much preceding cough, a gush of nearly 
pure blood or blood freely mixed with ordinary sputum. The 
blood is bright red, not dark or prune juice in appearance, and the 
liquid is forthy, while the cough, which is always present after the 
hemorrhage has occurred, is suppressed and resisted by the patient. 



THE SPUTUM 475 

who fears further bleeding. This hemoptysis may be caused, first 
by pulmonary tuberculosis; second, by valvular cardiac disease, 
generally involving the mitral valves; third, in pulmonary infarc- 
tion; fourth, by aortic aneurysm; fifth, by bronchiectasis; sixth, 
in persons suffering from severe purpura; seventh, in persons 
suffering from hemophilia. 

Bloody sputum must be separated from bloody vomit due to 
gastric hemorrhage arising from ulcer or cancer. (See Vomiting.) 
This can be done by the cough, by the frothy character of the 
expectoration, by the presence of physical signs in the lungs, and 
by the history of pulmonary disease. It may, however, be con- 
fused with slight hemorrhage from a dilated and ruptured vessel 
on the posterior pharyngeal wall, in which case, after a little cough- 
ing, there may be expelled on a handkerchief a little blood-tinged 
saliva. Examination of the throat will usually reveal the ruptured 
vessel or other vessels dilated, but still intact. For a number of 
days after an attack of hemoptysis there may be expelled in the 
sputum dark clots of blood. So-called "currant- jelly" clots are 
expelled by coughing in many cases of malignant growths of the 
lungs. 

Other causes of blood-streaked sputum are aortic aneurysm with 
leakage by oozing into a bronchus or the trachea; and particularly 
in children do we see streaks of blood in the sputum if there be 
present pulmonary gangrene. 

Care should always be taken to discover whether the materials 
spat up are really tinged with blood, for they may be colored by 
some dyestuffs or the blood, of some animal for the purposes of 
deception. 

Finally, it is well to remember that a reddish-brown or brick- 
dust looking sputum is sometimes coughed up in cases of hepatic 
abscess communicating with the lung; and the sudden expectora- 
tion of a brownish, purulent-looking sputum by a person who 
has been a sufferer from dysentery should cause the physician to 
examine the sputum for the ameba coli, in order to discover if 
the case is one of pulmonary abscess secondary to amebic dysen- 
tery. Symptoms of hepatic abscess will also be present. This 
has been called " anchovy-sauce" sputum. 

In adition to the sputum already described we sometimes see a 
peculiar semiliquid sputum in cases of pulmonary phthisis, in which 
the sputum promptly separates into two layers on standing, the 
upper one being light and rlocculent, unless there is a well-marked 
bronchial catarrh present, when it may be markedly mucopurulent. 
If a large cavity is present, its purulent character may be very 
marked. To this list may be added several others, namely, the 
purulent sputum of pulmonary abscess or empyema, of medias- 
tinal abscess opening into a bronchus, subphrenic abscess, hepatic 



476 



COUGH AXD EXPECTORATION 



abscess, pronounced bronchiectasis, and that from a large tuber- 
culous cavity in the lung. Of these the more common are bron- 
chiectasis, tuberculous cavity, and empyema breaking into a 
bronchus. In the first of these the cough is paroxysmal, and after 
it has been kept up for some time a gush of purulent sputum is 
suddenly brought up into the mouth, and the accumulation of pus 
is removed for a time. In the other the sputum is very fluid, and 
is so free that its expectoration rapidly fills the spit-cup, provided 
that the patient is strong enough to bring it up. A very frothy 
watery sputum occurs in pulmonary edema, particularly that seen 
in cases of Bright's disease, or heart failure, and in some of the 
pulmonary forms of epidemic influenza. It is often slightly blood- 
tinged. 




Fig. 160. — Curschmann's spirals. (Von Xoorden.) 

Sputum which on standing separates into three layers, the top 
one frothy and dirty looking, the next clear and filled with shreds, 
and the lowest consisting of a sediment of pus and broken-down 
looking materials, is seen in cases of pulmonary gangrene. If the 
sputum when placed in a vessel containing water sinks to the 
bottom in disk-like masses or globules the disease may be tuber- 
culosis. 

The sputum expelled by an asthmatic at the time of the attack 
also has characteristics not so easily seen at a glance, but never- 
theless demonstrable by the naked eye. Small pearls or plugs 



THE SPUTUM 477 

of mucus of the size of a sago-pearl are seen in the sputum, and if 
these are placed on a plate of glass under which is a black surface, 
and then teased out, they will be found to be rolled-up fibres, 
which when unrolled are found to be in the forms of curls or spirals. 
These are sometimes called Curschmann's spirals (Fig. 160), 
and they are rarely seen in several other conditions than asthma, 
namely, in chronic pulmonary tuberculosis and croupous pneu- 
monia. Through the central core of the curl runs a bright and 
refractive filament, which is waxy looking, and is probably not 
an entity, but an optical effect. Between the spiral fibres can be 
seen in many cases slight, bluish, octahedral crystals varying 
greatly in size, sometimes requiring a high-power lens to dis- 
tinguish them. They are said by Salkowski to be composed of a 
mucous substance, but others believe them to be oxalate of lime, 
a phosphate of an unknown base, or ethylenimin. These are 
called Charcot-Leyden crystals, and are also rarely seen in the 
sputum of chronic croupous pneumonia, chronic pulmonary tuber- 
culosis, and in acute bronchitis. 

Sometimes, in cases of diphtheria, casts of the larynx and upper 
bronchial tubes are expelled by coughing. Small casts are also 
seen in the sputum of that rare affection, fibrinous bronchitis. 
These casts may consist of a perfect mould of several branching 
bronchial tubes and bronchioles, and they may be white, yellowish, 
or even pinkish in color from bloody exudation. Sometimes they 
are only visible to the naked eye if placed in water and shaken, 
when what has appeared to be a roll of mucus spreads out into the 
characteristic shape of the tubes from which it comes. Casts of 
the finer tubes can sometimes be found in the sputum of cases of 
croupous pneumonia. 



CHAPTER XX. 
PAIN. 1 

The kinds of pain — The significance of its locality — Colic. 

It is manifest that it is impossible to enumerate all kinds of 
pain, both- as to its situation, degree, and character. Mention 
can be made only of those pains which possess considerable diag- 
nostic importance. It should always be remembered that pain is 
the sign adopted by Nature to notify the individual of some 
abnormal condition in his body, and in many instances pain is 
only developed when the attempt is made to move a part which 
from its condition had much better be allowed to rest. 

Pain is generally described as darting or stabbing in character, 
when it occurs in single or repeated paroxysms; as throbbing or 
pulsating, when it rises and falls in severity with the pulse beat; as 
dull and aching, when it resembles the feeling associated with a 
bruise. Sometimes stabbing or darting pains are called lancinat- 
ing, or the patient may state that the pain is tearing and rending 
in character. 

Not infrequently darting or stabbing pain is associated closely 
with actual disease of nervous tissue, which may be primary or 
caused by the pressure or irritation of a growth or some foreign 
body. Such pains are seen in inflammation of the sheath of a 
nerve or its surroundings as it passes through a bony foramen; 
in meningeal thickening; in the lightning or tearing pains of loco- 
motor ataxia; from pressure upon the spinal nerves by spinal 
disease or in that caused by fractured bones. Again, we often 
meet with violent pain as the result of true neuritis, whether it be 
produced by infection, by injury, or by poisoning. 

Throbbing pain is nearly always associated with the presence of 
congestion or local swelling in the part where the pain originates, 
and arises from the fact that the peripheral nerves are subjected 
to pressure, which is increased with each additional beat of the 
heart. Dull, aching pain is often produced by slow inflammatory 
or pathological processes in organs not well endowed with sensory 
nerves. 

There are two forms of pain yet to, be considered which are 
peculiar in their character, namely, that nauseating pain due 

: See also chapter on Headache. 



pain 479 

to a blow or injury to the testicle or ovary and that boring pain 
which occurs in cases of inflammation or morbid growth affecting 
bony tissues, particularly in the long bones. 

Pain is often referred to a point far away from the source of 
the symptom. Thus, the child with hip disease complains of 
pain in the knee or in the ankle; the one with dorsal caries, of 
pain in the intercostal nerves anteriorly; and a stone in the kidney 
may cause violent pain in the penis or testicle. So, too, a child 
suffering from pericarditis refers the pains to the epigastrium and 
very frequently the pain of appendicitis is thought to exist in the 
gall-bladder or to be due to a pleurisy. 

The physician should always remember that the degree of pain 
must be determined in part by the expression of the face and 
movements of the body, for often these features of a case will show 
that the pain described so vividly in words is much exaggerated. 
The general systemic signs of pain are a tense pulse, if the pain 
be recent in onset and acute; a somewhat accelerated respiration 
unless the pleurae or lungs are involved, when it may be retarded; 
dilatation of the pupils; more or less sweating, particularly on the 
forehead; faintness; and sometimes the passage of clear, limpid 
urine if the pain be abdominal. 

Neuralgic pains depend upon one of three causes, and, though 
they may occur in any nerve of the body, are most commonly seen 
in the nerves of the head; or in nervous women in the nerves of 
the pelvic organs and external genitals. The three causes are 
generally debility with anemia, reflex irritation, and irritation of 
the nerve by systemic poisons or by the presence of growths. 

Violent neuralgia of the head is commonly seen in overworked 
or overdanced women, who lack sufficient sleep and fresh air 
and who are anemic. It also arises from the reflex irritation of 
a decayed tooth, or from inflamed or overstrained eyes, or from 
a diseased ear, so that an examination of any one of these parts 
may reveal the cause of an obstinate neuralgic pain. Similarly 
we see cases of neuralgia, particularly of the supra-orbital nerve, 
which are due to chronic poisoning by one of the metallic poisons, 
such as lead and aresenic, and also as a result of malarial infection 
(brow ague). If the neuralgic pain be due to neuritis, it will not 
only be typical of neuralgia, but along the track of the nerve 
marked tenderness will be developed on pressure, and rarely an 
eruption will appear on the skin, as a herpes zoster. Pure neuralgic 
pain, in distinction from neuritis, on the other hand, is often 
relieved by pressure upon the nerve involved. 

When the fifth cranial nerve is affected by neuralgia, we find that 
if the upper branch is involved the pain is felt in the forehead, the 
eyebrow, and the eyeball, the conjunctiva often becoming injected. 
If the pain be in the upper lip, the posterior nares, and the check. 



480 



PAIN 



the infra-orbital or second branch is affected; while if the pain is 
in the lower jaw and chin, the third division of the fifth nerve is 
involved (Figs. 161 and 162). 

A peculiar form of neuralgic pain coming on in attacks or par- 
oxysms of great severity is migraine or megrim, in which the pain 
is usually confined to one side of the head, associated with great 
tenderness of the scalp, and may be preceded in many cases by 
disorders of vision, such as hemianopsia or dimness of visual 
perception. Associated with this pain at its zenith we frequently 
see vomiting and retching, faintness, with sweating localized in 
the pain area, or diffused, and great facial pallor. Pressure by the 



Fig. 161 



Fig. 162 




Showing the distribution of the three branches of the fifth nerve. 



fingers upon the painful area often produces no more pain or even 
gives partial relief, but a light touch may cause increase in the pain. 
Rarely a somewhat similar condition to migraine, which is not 
unilateral but bilateral, is found in connection with rheumatism 
of the scalp. As migraine may be due to a rheumatic state, care 
in making a differential diagnosis is necessary. The pain of migraine 
is, however, unilateral, more severe, more transitory, and associ- 
ated with the symptoms named, whereas in the rheumatic head 
pain the history of rheumatic tendencies of a marked character, 
the diffuse pain, the increased soreness on exposure to cold or 
changes in the weather, aid in separating it from migraine. (See 
chapter on Headache.) 



PAIN 451 

When syphilis or injury causes a periostitis of the skull, violent 
pain of a neuralgic character may be present, particularly at night, 
but the local symptoms are manifest, and when compared with 
the history make the diagnosis possible. 

It is also necessary to separate the headache of cerebral tumor or 
cerebral abscess from neuralgia of the head. The pain of such a 
cerebral condition is constant; the headache is sometimes worse at 
night, sometimes in the daytime, and greatly increased by physical 
or mental effort. The danger of confusing the pain of neuralgia 
with that due to tumor is great unless the physician remembers 
that the constant pain of tumor may vary from slight headache 
to sharp paroxysms of pain. The occurrence of convulsions points 
strongly to tumor if associated with headache of this character, 
and, finally, the presence of tumor as a cause of headache and not 
ordinary neuralgia is decided by evidences of optic neuritis, vomit- 
ing, vertigo, and the development of focal symptoms of localized 
paralysis. (See chapters on Headache, Vomiting, Convulsions, and 
Spasm.) 

The most common seat for neuralgic pain in the head, other than 
in the brow, is the occipital region, the posterior branch of the 
second cervical nerve or great occipital being the one most affected. 
As this nerve supplies the occipital region and the posterior part 
of the parietal regions, these areas may be involved in the painful 
manifestations, and all these parts may be tender to the touch. 
Brushing the hair may be impossible, because of the pain produced 
by the brush touching the scalp. Occipital neuralgia is often- 
times bilateral. It may simply arise from cold or injury; but, if 
persistent and severe, caries of the cervical vertebra should be 
sought for as a possible cause. 

Pain of a neuralgic or darting character in the neighborhood of 
the heart is found as the result of several causes, as a rule in the 
following order of frequency: (1) Pain with palpitation of the 
heart from the accumulation of flatus in the splenic flexure of 
the colon just as it turns to descend. Many patients who come 
to the physician complaining of heart disease suffer only from 
this condition, due to gas in the large bowel. Again, the pain 
due to gastric ulcer, or, as it has been called, cardialgia, may be 
referred to the heart by the patient. (2) To intercostal neuralgia 
due to debility or goutiness. In these cases a tender spot will 
often be found, one in the precordium, another in the outer edge 
of the scapula, and a third on the vertebral column. These are 
sometimes called the " spots of Valleix." In other cases the pain 
will be due to spinal disease, anemia, or the tight lacing of corsets. 
(3) To pseudo-angina. (4) To true angina pectoris. (5) To 
locomotor ataxia. 

Pain of a character somewhat resembling true angina pectoris is 
31 



482 PAIN 

also sometimes met with in patients who have that not rare disease, 
acute aortitis. The pain is often constant under the sternum, but it 
may have terrible exacerbations, and a sensation of rending of the 
retrosternal tissues. Death may occur in an attack. It is seen 
chiefly in gouty patients and in syphilitics. Very rarely it is seen 
in patients who have suffered from malarial poisoning. Pain is 
felt much more commonly in disease of the aortic orifice than in 
lesions of the mitral orifice of the heart. 

Pseudo-angina occurs most commonly in anemic, nervous girls, 
or young women whose vessels are normal but who have hysterical 
tendencies. The pain is not associated with marked changes in 
the circulation, the heart feels distended rather than compressed, 
and there is often borborygmi and hysterical belching. 

True angina occurs in those of middle age or advanced life or 
in young persons whose vessels are affected by syphilis. The 
bloodvessels will usually be found hard and corded, fibroid, and 
the blood-pressure high. The additional diagnostic points in 
favor of true angina pectoris are that the principal seat of pain 
is somewhat to the left of the lower and middle sternum, from 
which spot it may extend to the axilla and back and turn off to 
the occiput or extend down the arms, particularly the left arm, 
to the hands, where a sensation of coldness may be felt. Some- 
times even the abdominal organs and testicles seem to be affected. 
The patient is motionless, the face anxious and covered with a 
cold sweat, and respiration is shallow. The disease is usually 
seen in persons over forty years of age. The thoracic pain of 
locomotor ataxia is rarely felt in the precordium, but commonly 
in the axilla, and it rarely radiates down the arm. The other 
symptoms of tabes dorsalis should be sought for in all doubtful 
cases. (See chapter on the Legs and Feet.) True angina pectoris 
is far more rare in women than in men. 

Very severe pain, paroxysmal or constant, felt in the chest may 
also be due to aortic aneurysm, and, if so, will be found associated 
with pain shooting down the arm on the same side, dilatation of 
the pupil, unilateral sweating of the face and neck, and the 
physical signs described in the chapter on the Thorax. 

Severe pain of a darting character felt in the chest, not due to. 
angina or the causes just named, is nearly always an indication 
of one of four things: (1) Intercostal neuralgia, already named; 
(2) pleuritis, with or without pneumonia; (3) pericarditis, if it 
is felt in the precordium; (4) a morbid growth in the chest, par- 
ticularly a mediastinal tumor, or enlarged bronchial glands. 

Both intercostal neuralgia and pleurisy are associated with 
severe pain, increased by taking a deep breath, the pain occurring 
sometimes with inspiration and sometimes with expiration. They 
are to be separated from one another by the presence of cough, 



PAIN 483 

fever, and of a friction sound in pleuritis, and by the fact that 
the entire side is more or less tender to the touch in this state. 
When the pain is constant and lasts for a long time, it may be 
due to a low-grade pleuritis, resulting from pulmonary tuberculosis, 
particularly of the apex of the lung, the morbid process affecting 
the pleura. 

Pericarditis is frequently caused by rheumatism, more rarely 
by pneumonia, and the pain is felt in the precordium. (See chapter 
on Thorax.) 

Pain felt at the right of the left scapula or between the shoulders 
is often due to gastric ulcer or dyspepsia. 

The pain of mediastinal growth is due to pressure on nerve 
trunks, and the diagnosis may be very difficult unless bulging and 
dulness on percussion are present. The condition is rare. 

Neuralgia of the pelvic viscera in women is frequently seen as 
the result of functional or organic disease. It may be ovarian, 
when it is very apt to occur with greatest severity half-way between 
the menstrual epochs or just before them. Sometimes the neu- 
ralgia may be present in the labia majora or in the perineum. It 
usually occurs simply as a sudden, darting pain, which does not 
last, and, indeed, rarely continues more than a moment, although 
there is usually associated with it more or less constant uterine 
or ovarian tenderness. Care should be taken that these pains 
are not thought to be due to cancer or other severe organic 
lesions. 

Pain in the sacral region is often an indication of uterine or 
rectal disease. If higher up the back, it is often due to myalgia 
or lumbago; and lumbago, if not due to rheumatic tendencies, 
is often due to the colon being loaded with feces. More or less 
constant pains in the lower dorsal region is commonly found as a 
complication of enteroptosis and is relieved by proper support. 
Backache also is often due, particularly in women, to strain of the 
sacroiliac joint. Such pain often radiates down the backs of the 
thighs and gives rise to the diagnosis of rheumatic lumbago and 
sciatica. It is not relieved by salicylates, but is relieved by strap- 
ping, the use of shoes without high heels, and proper corsets. 

If the patient is a child, pain in the back should cause us to 
suspect spinal caries, rickets, or scurvy. If the former, any jar 
will greatly increase the pain; but if the child be placed over the 
knees, face downward, and the knees separated so that inter- 
vertebral pressure is removed, the pain disappears. Such a child 
if told to jump down from a stool will not obey, but will take care 
to slide off gradually and gently on to the floor, in order to avoid 
jarring the spine. 

In scurvy the tenderness of the spine is usually diffuse, and it 
may mislead the physicians into a diagnosis of spinal disease, but 



484 PAIN 

investigation of the gums will reveal scorbutic blebs and the diet 
will be found imperfect. (See chapter on the Lower Extremities.) 

When a patient suffers from violent pain, increased by motion, 
extending from the sciatic notch in the buttock down the posterior 
part of the thigh, even to the ankle or heel, the pain signifies an 
attack of sciatic neuralgia in an adult, or if it occurs in a child 
gives grave reason for suspecting hip disease. If it is not sciatic 
neuralgia, it is due to sciatic neuritis, or, rarely, to a growth in the 
pelvis pressing upon the nerve before it emerges from the pelvis. 
The pain is fairly constant, generally worse at night, and becomes 
agonizing at times, even if the patient remains absolutely quiet 
and does not move the limb. The following points will, when 
pressed on, increase the pain if it be neuritis: the point of exit of 
the nerve from the pelvis, on the lower part of the sacrum, the 
head of the fibula, and behind the malleolus on the outside of the 
ankle. If these points are found, combined with a history of 
exposure to cold, injury to the nerve, rheumatic tendencies, and a 
persistency and tendency to return, the diagnosis of sciatica is 
clear. If the pain be due to sciatic neuritis there may be found 
wasting in the muscles supplied by the nerve, and some anesthesia 
of the skin, and herpetic eruptions may appear on the skin along 
the course of the nerves. There will be also a history of long 
duration, and the leg will be apt to feel numb and tense from 
effusion into the sheath of the nerve. (See chapters on the Skin 
and on the Feet and Legs.) The heel and toes will be tender, 
but the inner aspect of the plantar surface will usually escape. 
Again, in sciatic neuritis, if the leg be extended, and then while 
in extension flexed at the hip, pain will be felt at the sciatic notch. 
When the pain is a pure neuralgia, which is rare, it is not increased 
by moving the limb, there is little or no tenderness on pressure on 
the nerve trunk, and the patient often suffers from neuralgia of 
other nerves. 

Sciatica is much more common in men than in women, which 
is the reverse of all other nerve pains of like character, and far 
more usual in middle or advanced age than in the young, in whom 
it is almost unknown. 

Double sciatic pain should arouse suspicion of locomotor ataxia, 
of malignant growth pressing on the spinal cord or on both nerves 
in the pelvis, the presence of lumbar abscess or of diabetes mellitus 
causing neuritis. 

When there is an hysterical, painful joint at the knee or hip in a 
woman, care is necessary to discover that the pain is over the entire 
leg rather than in the course of the nerve. Care must also be taken 
that rheumatism of the muscles of the thigh be not taken for 
sciatica. This can be separated from sciatica by the diffuse 
character of the pain and tenderness and by the fact that in the 



PAIN 485 

rheumatic condition the slightest muscular pressure causes pain. 
Sometimes a malignant growth of the femur may produce symptoms 
of sciatica. I had a case of osteosarcoma of the femur which had 
been treated for sciatica for several months. 

Finally, renal calculus may cause violent pain to be felt down 
the thigh. (See below.) 

It should also be remembered that malingerers, particularly 
soldiers desiring to shirk duty, often pretend to have sciatica. 

Abdominal Pain. — Abdominal pain of sufficient severity to 
cause a patient to seek medical aid may be due to a large number 
of causes. Its locality is of some value in helping to determine 
its cause, but too much reliance should not be placed upon the 
statements of the patient as to its site, because even the most 
intelligent may be unable to correctly indicate its actual point 
of origin. In a general way it may be stated that a pain which is 
most severe in the upper right quadrant of the abdominal area 
is probably gall-stone colic, or cholecystitis, or rarely disease in the 
pyloric portion of the stomach. So, too, pain in the right lower 
quadrant is probably due to appendicitis, or it may be due to 
carcinoma of the caput coli, and in women, to disease of the ovary 
or Fallopian tube. Pain in the upper left quadrant is most com- 
monly due to flatus at the splenic flexure of the colon and rarely 
to gastric ulcer, while pain in the left lower quadrant is due to 
gas, to a growth in the bowel or to a sigmoiditis, or to ovarian or 
tubal disease. 

By far the most frequent form of abdominal pain is that due 
to flatus arising from indigestion. A peculiarity of this form of 
pain is the fact that it is rarely limited to one spot for any length 
of time, and is usually relieved by the passing of gas from the 
rectum. It may be associated with diarrhea and a history of the 
ingestion of indigestible food. Further than this, percussion will 
elicit a tympanitic note in the area of greatest pain and distention, 
whereas, in intestinal obstruction due to tumor or intussusception, 
percussion may reveal dulness and a mass may be felt. (For 
the various forms of intestinal obstruction, see the chapter on 
Vomiting.) 

In hepatic colic the patient often, after some days of wretched- 
ness and " biliousness," is seized by sudden and violent pain in 
the right hypochondrium, which is paroxysmal in character. 
Jaundice ensues in some cases with more or less rapidity, and 
fever of an irregular type may occur. It is worthy of note that a 
gall-stone when in the gall-bladder, or cystic duct, rarely causes 
much pain, and its impaction in this duct does not cause jaundice. 
If it be in the hepatic duct jaundice is present, and pain is often 
marked, but is not so severe as if it be in the common duct. (See 
chapter on Abdomen.) 



486 PAIN 

If the stone be impacted in the common duct, then the most 
violent pain is present, and jaundice is marked, as a rule, the 
stools being clay colored. If the symptoms develop suddenly, 
and pass away equally rapidly, the stone has probably escaped 
into the bowel, whereas if the stone becomes impacted in the 
papillae of the duct, the jaundice and other symptoms become 
progressively worse, although the pain may diminish. It is entirely 
possible for the same stone to slip back, and cause temporary 
relief, then to slip into place and precipitate another attack, or 
for another calculus to follow its predecessor, causing a return of 
the symptoms. Pain is more indicative of stone than any other 
cause of obstruction of the common or cystic duct. Thus, in 80 
cases of common-duct obstruction pain was marked in 51, absent 
in 10, and unrecorded in 19, while in 79 cases due to other causes 
than stone, pain was present in only 9. 

If the stone is movable, there may be attacks of acute radiating 
pain with chills, and sweats due to sepsis from the damaged mucous 
membrane. (See Charcot's Fever.) 

Boas has pointed out that in many cases of gall-stone a spot of 
tenderness may be found at the level of the twelfth dorsal vertebra 
three inches to the right of the vertebral line. 

Severe pain in the hepatic region may also be due to acute 
cholecystitis. There is usually local muscular rigidity, tenderness, 
and vomiting, but the liver is not enlarged unless the cholecystitis 
is associated with cholangitis. This condition complicates gall- 
stones or follows the infectious fevers, notably typhoid fever, 
and may be confused with appendicitis, which may cause abscess 
behind the liver. The pain often comes on in paroxysms, and is 
associated with fever, enlargement of the gall-bladder, and great 
tenderness in its area on palpation. The liver itself is not enlarged. 
If suppuration is present, the symptoms of general sepsis may 
develop. The paroxysms of pain may be very like those of gall- 
stone in the endeavor of the gall-bladder to extrude its thick 
mucopurulent contents. Care should be taken not to mistake a 
subphrenic abscess for cholecystitis. 

The pain of diffuse hepatitis varies with the severity of the 
inflammation, and it may not be present unless the hypochondrium 
is palpated. 

When there is a history of violent colic situated near the hypo- 
chondrium, or in the epigastrium, not accompanied by jaundice 
and enlargement of the liver, the possibility of the cause being a 
pancreatic calculus is not to be forgotten. Such a condition is very 
rarely met with, and still more rarely do we find pancreatic stones 
in the feces, because they are friable and broken up in the bowel 
before they are passed. Boas states that they are a frequent 
cause of so-called " neuralgia of the liver." It should not be 



PAIN 487 

forgotten that blocking of the common duct by gall-stone also 
produces blocking of the pancreatic duct, and this in time may 
cause a complicating attack of acute pancreatitis. 

The pains just described are so severe and characteristic in 
their distribution that they cannot well be confused with those of 
intestinal indigestion, in which condition we have a history of the 
ingestion of bad food, a state of more or less flatulent distention 
of the entire belly, and, it may be, diarrhea. 

The pain arising from the presence of a gastric ulcer may, with 
its associated symptoms, so closely resemble that due to chole- 
lithiasis as to make a differential diagnosis almost if not quite 
impossible. The same statement holds true of duodenal ulcer. 
The pain of all these affections may be so near the area of 
the biliary passages that its localization by the patient gives 
the physician no aid whatever. Jaundice is so often absent 
in cases of hepatic colic that its absence in no way excludes this 
state. While the presence of an excess of hydrochloric acid in the 
gastric contents points to ulcer it sometimes occurs that hyper- 
acidity arises from reflex irritation from the gall-bladder. Even the 
development of pain after the stomach is empty, due to the irritating 
effect of the acid upon the gastric ulcer, may also develop in cases 
of gallstone if there has developed around or about the gall-bladder 
inflammatory exudations and adhesions which interfere with the 
movements of the pylorus and duodenum as the food passes into 
the small bowel. The presence of hematemesis is strongly indicative 
but not pathognomonic of ulcer. The relief of pain produced by 
taking food, tenderness on deep palpation of the epigastrium, the 
presence of a hyperesthetic spot in the skin over the stomach are 
also indicative of ulcer. (See chapter on Abdomen.) 

In pancreatitis the pain is sudden in onset, violent, and usually 
felt chiefly in the left upper zone of the abdomen. The belly is 
distended, nausea and vomiting are present, and fever may be 
present also; delirium may come on, and death generally speedily 
ensues unless operative measures are resorted to. (See Abdomen.) 

Very rarely severe abdominal pain with vomiting, diarrhea, and 
even the passage of blood may be the result of angioneurotic edema 
with an abdominal crisis. This pain is usually diffused through- 
out the belly and not confined to one area, although at onset 
it may be in the epigastrium. These symptoms may seriously 
mislead the surgeon unless he first makes inquiries, designed to 
discover the fact that attacks of angioneurotic edema have affected 
other parts of the body. This is the more important, in view of the 
fact that these attacks are often precipitated by indiscretions in 
diet as is appendicitis and gall-stone colic. The skin should always 
be carefully examined to discover traces of urticaria. 

The sudden development of pain oi great intensity in the right 



PAIN 



lower quadrant of the abdomen (see McBurney's point, Fig. 163), 
associated with muscular rigidity of the abdominal wall, tenderness 
on palpation, a quick pulse, a rise of temperature, and in some 
instances vomiting indicates the development of appendicitis, a 
diagnosis which is aided, but not confirmed, if on examining the 
blood a distinct leukocytosis is present. It is worthy of note that 
the pain of appendicitis is often referred in its greatest intensity, 




Fig. 163. — The black spot is at "McBurney's point. " 

and by intelligent patients, not to the neighborhood of the appendix, 
but to the epigastrium, or even to the region of the sigmoid flexure, 
and it is by careful palpation only that the area of greatest tender- 
ness is found in the appendicular region. 

Before reaching a diagnosis of acute appendicitis the physician 
must exclude the following causes of pain referred by the patient 
to the appendicular area. One of these is diaphragmatic pleurisy; 
another is subphrenic or ovarian or tubal disease if the patient 



PAIN 489 

be a woman. Rarely a floating kidney, or hydronephrosis, may 
be provocative of similar symptoms, as may also phlebitis of the 
iliac vein. If the pain is very severe, so severe that the patient 
is incapacitated from giving a clear description of its chief seat, it 
may be due to gall-stones, renal stone, or intestinal perforation. 
Severe pain may also be due to inflammation or twisting of 
Meckel's diverticulum. 

Generally diffused pain of a constant severe character felt all 
over the abdomen or localized at first in some particular spot, 
and greatly increased by pressure, should lead the physician to 
examine the case for a possible peritonitis. Nothing else causes 
such violent, diffuse pain. The well-flexed legs, the anxious face, 
the drawn upper lip, quick pulse, the exquisitely tender abdominal 
surface, the thirst, the moderate fever, and the rapid onset of 
collapse in fatal cases render the diagnosis easy. 

The onset of severe pain in the abdomen in the course of typhoid 
fever, while not necessarily an indication of perforation of the 
bowel, is nevertheless deserving of careful study. If it is due to 
perforation, as a rule it is violent enough to make the patient cry 
out if he be not stuporous, and the following symptoms will prob- 
ably be present in whole or in part: The temperature will sud- 
denly fall greatly, the epigastrium and general abdominal wall 
will be fixed and the abdominal wall may be scaphoid or dis- 
tended. Percussion of the area of the liver may show obliteration 
of hepatic dulness, as a result of gas being between the wall and 
this organ, but while this is an important sign if present, its 
absence does not in the least exclude perforation. Hiccough 
may be present, and perhaps vomiting. The facial expression 
is that of grave abdominal disorder. (See chapter on the Face.) 
As in suspected appendicitis so in suspected typhoid perforation, 
the chest must be carefully examined lest the pain of an acute 
pleurisy be mistaken for abdominal disorder. So, too, it is essential 
that the pain of acute cholecystitis, appendicitis, and renal calculus 
be excluded before a diagnosis of perforation is determined. 

Sometimes a patient who has floating kidney will suffer from 
severe renal pain, nausea, vomiting, and collapse, the symptoms 
simulating renal calculus. These attacks are known as Dietl's 
crises. 

If the pain be due to chronic lead poisoning, it centres about the 
umbilicus, and is of a twisting, knotty character, "as if the bowels, 
were being twisted around a stick." There is a history of exposure 
to lead in many cases, and a blue line on the gums can often be 
found. 

If due to fecal impaction, there is a history of a continued tendency 
to constipation, with dry, hard stools, and a lump oi hardened 
feces may perhaps be felt through the belly wall. 



49° PAIN 

If due to intestinal obstruction, the pain has no characteristic 
seat in any part of the abdomen, as a rule; but the general symp- 
toms of this condition will be found present in the case. (See 
chapters on Vomiting and on the Abdomen.) 

Abdominal aneurysm may cause severe pain by pressure on 
nerve trunks; and uterine and peri-uterine disease also cause, 
reflexly, epigastric pains. 

Reference has already been made to the pain of renal colic. 
The characteristic symptoms of this condition are as follows: 
In renal colic the patient is suddenly seized with violent pain in 
the region of the kidney on one side, which passes down to the 
groin and even to the end of the penis. It is paroxysmal in char- 
acter, and so excessively severe that it often produces sweating, 
vomiting, and even fainting. The condition is seen much more 
frequently in men than in women. , The pain often suddenly 
subsides, leaving only a sense of soreness and tenderness in its 
track. The urine may be partly suppressed and bloody if the 
stone injuries the ureter to any great extent. 

Pain simulating renal colic may, however, be due to neuralgia 
or arise from several organic causes not connected with calculus. 
Thus, Habershon has stated that in valvular disease of the heart, 
particularly of the aortic valves, severe and colicky pains frequently 
radiate down into the right hypochondriac region, and Ralfe 
says into the renal region. Again, pain in this part may be due 
to aneurysm of the aorta or of the mesenteric artery. Further, 
the accumulation of hard fecal matter in the colon may cause 
nephralgia. Finally, Ralfe calls attention to the renal pain felt 
generally in the right kidney by women who have exercised violently 
while wearing a tight corset, which has pressed upon the liver 
and kidney with great force on making a jump or a sudden bend 
of the trunk. Sometimes a sudden "storm" of uric acid or an 
accumulation of oxalic acid in the kidney causes pain and tender- 
ness. Occasionally a tuberculosis of the kidney or a pyelitis may 
cause renal colic by the passage of a cheesy plug into the ureter. 

The presence of constant pain and soreness in the abdomen 
on one side, frequent micturition, and occasionally the presence 
of blood in the urine, are symptoms of several renal states, such 
as pyelitis, renal calculus, a tumor in the renal pelvis and tuber- 
culosis of the kidney. The pain is chiefly in the region of the kidney 
and along the course of the ureter where it crosses the pelvic 
brim; and as it is often made more severe by standing and is of a 
bearing-down character, it may be thought in women to be uterine. 
Jolts or jarring of the body also aggravate it, as does the act of 
urination. Sometimes a good deal of pain is felt on the sound 
side. 

If an examination of the urine reveals pus, this will indicate 



PAIN 



49 1 



pyelitis; and if the pus contains tubercle bacilli, tuberculous 
pyelitis. The latter diagnosis is confirmed if tuberculous disease is 
present in other organs, for renal tuberculosis is often secondary. 
Small cheesy masses may be present in the urine in the latter 
state. Renal calculus will be attended by attacks of renal colic, 
which, as a rule, are more severe than those produced by the 
passage of masses of broken-down matter along the ureter. A 
history of having passed a stone at some previous time, is of 
importance in the diagnosis. 

Some Abdominal Conditions in which Sudden and Acute Pain forms a 
Prominent Symptom. 1 



Disease. 


Mode of 
onset. 


Acute intestinal 
obstruction : 
a. Strangula- 
tion due to 
bands. 


Very sud- 
den. 


b. Acute intus- 
susception. 


Sudden 
to very 
sudden. 


c. Acute volvu- 
lus. 


Sudden. 


d. Due to gall- 
stone or 
stricture. 


Less sud- 
den, gra- 
dual. 


Appendicitis. 


Very sud- 
den. 


Acute peritonitis. 


Very sud- 
den. 


Hepatic colic. 


Sudden. 


Renal colic. 


Sudden. 


Intestinal colic. 


Sudden 

or 
gradual. 



Character of pain. 



In kind. 



In inten- 
sity. 



More or less 
continuous. 



Paroxysmal. 



Paroxysmal, 

but less than 

b. 

Paroxysmal 
later. 



Quite con- 
tinuous. 



Continuous. 



Aching, tear- 
ing, parox- 
ysmal. 



Aching, tear- 
ing, parox- 
ysmal. 



Paroxysmal. 



Most in- 
tense, 
agonizing. 

Severe. 



Moderate. 



Moderate. 



Agonizing 



Very severe 



Agonizing. 



Agonizing. 



Varies in 
severity. 



Seat of pain. 



Epigastric or um- 
bilical region. 



Epigastric or um- 
bilical region. 



Umbilical .or over 
heart. 



Often near seat of 
obstruction. 



At first periumbili- 
cal, later about 
appendix. 

All over belly, but 
chiefly epigastric 
or umbilical. 

Epigastric, radi- 
ating to between 
shoulders or to 
shoulder-blade. 

Affected loin, pass- 
ing down in front 
into testicle and 
bladder. 

Varies in position. 



Tenderness and 
pressure. 



Pressure at first re- 
lieves, afterward 
aggravates. 

Pressure at first re- 
lieves, afterward 
aggravates. 

Pressure never 
causes pain. 



Tenderness over 
obstruction. 



Greatest over ap- 
pendix or in left 
groin. 

Very tender every- 
where except at 
very first. 

Pressure at first re- 
lieves, then un- 
bearable over 
gall-bladder. 

Tenderness over 
affected kidney. 



Relieved by press- 
ure. 



Pain in the abdomen of the darting neuralgic type, other than 
that due to gall-stones, renal calculi, ordinary gastralgia, lead 
poisoning, enteralgia, or malignant growth, may be due to loco- 
motor ataxia. This possibility should never be forgotten, and 



Andrews' table, slightly modified. 



49 2 PAIN 

the fact that the patient is an adult, complains of the most violent 
pain in the belly, and has no other abdominal signs, should make 
us search for the other signs of tabes dorsalis. Generally these 
attacks will be of a tearing, rending character; they may be beyond 
description in severity, and after they pass off the patient is left 
in a condition of nervous wreck. Sometimes the pain is in the 
stomach, sometimes in the bladder. 

Grube has reported cases showing that diabetes may produce 
attacks of violent abdominal pain resembling the crises of an 
ataxia. 

Circumscribed abdominal pain of a constant character and gen- 
erally of less severity than that just described, may be due to an 
abdominal tumor (see Abdominal), or to ulcer of the stomach or 
bowel. 

In dysmenorrhea the pain is sometimes severe but it differs 
from that of inflammation in that it is paroxysmal and that there 
is no real tenderness on pressure; and, again, the patient does 
not lie still, but tosses from side to side in the bed. The pain of 
pelvic tumor is usually produced by pressure on a nerve, and is 
increased by palpation in some cases, as is also that of ovaritis. 
In cystitis the pain is deep in the pelvis, radiating upward, and is 
associated with tenderness, vesical spasm, and tenesmus. 

The pain of fissure of the anus is not at all proportionate to the 
lesion producing it. This pain may be atrocious and agonizing, 
and often is produced by a movement of the bowels, after which 
it lasts for some hours. 

(For abdominal pain due to conditions associated with move- 
ments of the bowels, see chapter on the Bowels and Feces.) 

Pain in the Feet and Limbs. — Pain in the ball of the foot at the 
base of the great toe, which is hot and exquisitely painful, is gout. 
Neuralgia of the toe and foot is a very rare condition, and is some- 
times called " Morton's painful toe," or metatarsal neuralgia. 
Severe pain at the base of the fourth toe comes on suddenly, and 
may radiate up the anterior aspect of the leg. Sometimes it is 
only dull, at other times it is so sharp and excruciating as to cause 
the patient to scream. It is separated from gout by the absence 
of any signs of inflammation in the part, by the fact that the big 
toe is not affected, and by the age and history of the patient. 
At times the base of the second toe is affected. Such a case will 
usually indicate that the patient has worn an ill-fitting boot. 

Pain in the foot and leg is often due to a broken arch of the 
foot. 

Finally, in connection with this class of cases there should not 
be forgotten two others, namely, those in which idiopathically or 
otherwise, growths form on nerves and cause pain; and, secondly, 
cases in which the arm or leg having been amputated, a neuroma, 



pain 493 

or catching of the end of the nerve in the scar, causes violent 
pain in the lost part, according to the patient's sensation, because 
the perceptive centres have been trained to regard pain impulses 
coming along this nerve as from its peripheral end. Thus a man 
whose leg may have been amputated years before will complain 
of severe pain in the amputated foot, although he knows it is off. 
(For Pain in the Arms and Legs, see chapters on these parts.) 

One of the most misleading forms of pain of a severe character, 
involving the entire body, with fever, delirium, and a variable 
skin eruption and swelling of the joints, may in the early stage 
be thought to be smallpox or rheumatic fever, when in reality it 
is due to dengue, or breakbone fever. 



CHAPTER XXI. 
TENDON REFLEXES AND MUSCLE TONE. 

The knee-jerk and ankle clonus — The arm-jerk — The significance of decreased 
and increased reflexes. 

I have already had occasion, particularly in those chapters 
devoted to the Legs and Feet and the Arms and Hands, to speak 
of what are called the reflexes or " muscle- jerks." There is much 
discussion as to whether the muscular contractions produced by 
tapping the tendon attached to a muscle are the result of a reflex 
action, in which the spinal cord is directly involved, or whether 
it depends upon muscle irritability or tone. It is not necessary 
for purposes of diagnosis to enter into a discussion of this char- 
acter, because the facts in our possession prove conclusively that 
variations of these muscle-jerks are of great diagnostic importance 
in diseases of the nervous system, whether they be true reflexes 
or not. The knee-jerk, or, as it has been called, the patellar reflex, 
is the diagnostic sign most frequently sought in studying nervous 
diseases associated with lesions in the spinal cord, because it is 
most easily developed. 

The methods of developing the knee-jerk, elbow-jerk, and 
ankle clonus have already been described in the chapters on the 
Hands and Arms and the Feet and Legs, to which the reader is 
referred. (See pages 71, 72, 108, and 109.) 

The chin- jerk is elicited by having the patient open his mouth 
slightly and then placing a flat object, like a paper cutter or tongue 
depressor, on the edges of the lower teeth. A sharp tap is now given 
to the flat object; when in health there will be a slight upward 
jerk of the chin. 

The scapulohumeral reflex of von Bechterew is elicited by tapping 
the skin on the spinal border of the scapula near its inferior angle. 
This usually causes a slight adduction and external rotation of the 
arm. It is exaggerated in neurasthenia, but its chief diagnostic 
value is in connection with lesions in the pyramidal columns 
above the cervical enlargement, in which state it is greatly altered 
in. that we now find contraction of the posterior fibres of the trape- 
zius, the deltoid, biceps, and forearm muscles, so that the shoulder 
is raised, the arm thrown from the side, the forearm flexed, and^ 
the fingers extended that the muscles on the opposite side also 



TENDON REFLEXES AND MUSCLE TONE 495 

respond. If the brachial plexus be diseased, the response on that 
side may be greater than on the side that is tapped. 

Having learned how to test these muscle-jerks, we now turn 
to a consideration of what they mean when absent or abnormally 
increased. 

A loss of knee-jerk is not characteristic of any disease unless 
this loss is associated with other symptoms which only need the 
discovery of this symptom to confirm the diagnosis. The nervous 
conditions in which we find the reflexes decreased or lost, taking 
the patella reflex as a type, aside from profound nervous exhaustion, 
are locomotor ataxia; peripheral neuritis; poliomyelitis, acute or 
chronic; transverse myelitis, if the disease involves the reflex arc; 
Friedreich's ataxia; diphtheritic paralysis; apoplexy, immediately 
after the shock; Landry's paralysis; spinal meningitis; spinal 
injuries, immediately after the accident; epilepsy, immediately 
after an attack; and chorea. We also find a total loss of reflexes 
in advanced diabetes mellitus and sometimes in diabetes insipidus. 

By far the most common cause of the loss of the knee-jerk is 
locomotor ataxia, but any lesion involving the posterior columns 
of the cord or the posterior nerve roots in the second, third, or 
fourth lumbar segment will produce the same results. Therefore, 
loss of knee-jerk is symptomatic of transverse myelitis of this 
region as well as of ataxia. Again, if the motor tract of the cord 
at these levels is diseased the knee-jerk is lost, as, for example, in 
acute and chronic poliomyelitis or myelitis involving the motor 
part of the reflex arc; and, finally, peripheral neuritis, which 
blocks the pathway from the periphery to the cord, and from the 
cord to the muscles, also causes loss of knee-jerk. 

If the cause of loss of knee-jerk be locomotor ataxia, we will 
probably find in addition to this symptom some difficulty in 
walking particularly if the eyes are shut; a lack of steadiness if 
the feet are placed together when the patient stands with his eyes 
shut; Argyll-Robertson pupils, or a reaction to accommodation 
but not to light; attacks of severe pain in the body or limbs; and, 
it may be laryngeal crises or spasms and atrophy of the optic 
nerve. 

If the cause of loss of knee-jerk be neuritis, we may find tender- 
ness on pressure along the nerve trunks, diminished muscular 
tone, and some wasting; an absence of any disturbance of the 
bladder and no Argyll-Robertson pupil, laryngeal or other crises. 
nor optic atrophy. 

Again, if the cause be acute poliomyelitis, there will be a history 
of sudden onset with fever, the limbs will be relaxed and flabby, 
the muscles will rapidly waste and become very feeble or paralyzed, 
and there will be no sensory symptoms whatever. The patient 
will usually be a child if the disease is acute. 



49^ TENDON REFLEXES AND MUSCLE TONE 

If the loss be due to transverse myelitis of the second, third, 
and fourth lumbar segments, the symptoms of paraplegia, paras- 
thesia, and anesthesia, with atrophy of the muscles and loss of 
control of the bladder and rectum, will be present, and a girdle 
sensation may be marked. 

In Friedreich's ataxia the history of heredity, the nystagmus, 
the early age of the patient, the absence of pupillary symptoms, 
the ataxic gait, and the loss of reflexes, are the facts which go to 
form our basis for a diagnosis. In the remaining diseases named 
the history of the case points to the cause of the loss of the knee- 
jerk very clearly. 

The conditions in which we rind the knee-jerk increased are 
apoplexy, sometime after the attack; disseminated sclerosis 
cerebral palsy of childhood; paretic dementia (not constant); 
primary lateral sclerosis; amyotrophic lateral sclerosis; ataxic 
paraplegia; hysterical paraplegia; transverse myelitis if the lesion 
is above the reflex arc; epilepsy some minutes after the attack; 
unilateral lesions of the cord on the paralyzed side; injuries to 
the spinal cord, after the recovery from first shock; pressure on 
spinal cord above the reflex arc; hereditary cerebellar ataxia; 
sciatica; tetanus; rheumatoid arthritis; and neurasthenia. 

The history of sudden paralysis and unconsciousness in a case 
of apoplexy with stertorous breathing, followed by loss of the 
knee-jerk, and then its return in an exaggerated manner, make 
the diagnosis clear unless the attack be one of the apoplectiform 
attacks of disseminated sclerosis, in which case there will be 
present a history of the intention tremor, nystagmus, and the 
syllabic speech, so that though the knee-jerk is exaggerated in 
both diseases the diagnosis can be readily made. In the cerebral 
palsy of childhood, the age of the patient, the contractures and 
gait, with the history, decide the diagnosis. In lateral sclerosis 
the spastic rigidity, excessive exaggeration of the knee-jerks, 
absence of sensory disturbances, and ocular symptoms, all render 
the diagnosis possible. Similar exaggeration is also seen in amyo- 
trophic lateral sclerosis, in which disease there is wasting of the 
muscles, particularly of the hand. In both these ailments the 
exaggeration of the knee-jerk is due to disease of the lateral 
pyramidal tracts, which block the inhibitory fibres from the 
higher centres. For similar reasons we find exaggerated knee-jerk 
in ataxia paraplegia. 

In hysterical paraplegia the age and sex of the patient, the 
peculiar facies, the areas of anesthesia and hyperesthesia, and the 
peculiar gait point to the diagnosis. 

The increased knee-jerk in cases of transverse myelitis occurs 
when the lesion is situated at such a point in the cord that the 
lateral tracts are cut off and the reflex arc is preserved. 



TENDON REFLEXES AND MUSCLE TONE 



497 



In neurasthenia the knee-jerks are exaggerated, but are easily 
exhausted. 

Leaving the knee-jerks as a type of a reflex, we find that the skin 
reflexes are often lost in cases of apoplexy when the deep reflexes 
are exaggerated. (See chapter on the Skin.) 

The plantar reflex obtained by tickling the sole of the foot has 
recently attained considerable diagnostic importance through the 
work of Babinski, who has found that in normal persons such 
irritation causes flexion of the toes on the metatarsus, whereas in 
disease of the pyramidal tracts extension of the great toe, with or 
without extension of the other toes, takes place, as, for example, 




Fig. 164. — Babinski reflex in health, somewhat exaggerated, 
drawn up toward the knee. 



The toes are 



in spastic paraplegia. The normal reflex, somewhat exaggerated, 
is shown in the figure. It is a noteworthy fact that in infants 
in health extension takes place instead of flexion, and that the 
administration of full doses of strychnine to adults will some- 
times reverse the normal reaction. The Babinski reflex is not 
pathognomonic of disease of the pyramidal tract, although it is 
indicative. 

In glossolabiopharyngeal paralysis the reflexes of the tongue 
and throat are lost and those of the face sometimes increased; in 
progressive muscular atrophy the reflexes of the arms are lost, 
while those of the legs are preserved; and in tuberculous meningitis 
the reflexes are apt to be more marked on one side than the other. 
32 



49 8 



TENDON REFLEXES AND MUSCLE TONE 



In athetosis the reflexes are increased in the affected part. 

Ankle clonus is found most marked in lateral sclerosis, in dissemi- 
nated sclerosis, and in amyotrophic lateral sclerosis. A false 
clonus is sometimes seen in hysteria. (See pages 107 to no.) 

A Table of the Skin Reflexes. 



Reflex. 


Point of stimulation. 


Situation of centre. 


Significance. 


1. Plantar, 


Irritating skin of soles. 


Extreme end of cord. 


Usual in health. 


2. Gluteal, 


Irritating skin of but- 
tocks. 


Origin of 4th and 5th 
lumbar nerves. 


Rare in health. 


3. Cremasteric, 


Irritating skin of inner 
side of thighs. 


Origin of 1st and 2d lum- 
bar nerves. 


Usual in health ; best 
marked in boys, on 
account of the newly 
formed cremaster. 


4. Abdominal, 


Irritating skin of abdo- 
men in line of nipples. 


Origin of 8th to 12th dor- 
sal nerves. 


Frequently absent. 


5. Epigastric, 


Irritating skin of chest 
In 5th and 6th spaces. 


Origin of 4th to 6th dor- 
sal nerves. 


May be absent in health. 


6. Erector spinse, 


Irritating skin from sca- 
pula to crest of ilium. 


Origin of all the dorsal 
nerves. 


Rare in health : frequent 
in wasting disease. 


7. Interscapular, 


Irritating skin between 
scapulae. 


Origin of 6th cervical to 
3d dorsal. 


Rare in health. 


8. Palmar, 


Palms of hands. 


Cervical bulb. 


Only in infants. 


9. Cranial: 

Conjunctival, 


Sclerotic, or inner sur- 
face of eyelid. 


Medulla. 


Absent in disease of 5th 
nerve only. 


Iris (to light), 


Pupil. 


Anterior portion of ocu- 
lomotor nucleus. 


Absent in disease only. 


Palate, 


Soft palate and uvula. 


Medulla. 


Absent in disease only. 


Nasal (sneez- 
ing), 


Naso-respiratory pas- 
sages. 


Medulla. 


Absent in disease only. 



INDEX 



Abadie's sign, 43 
Abdomen, 298 
distention of, 300 
frog belly, 300 
inspection of, 299 
localized bulging of wall of, 303 
pain in, 29, 484, 492 
palpation of, 309 
percussion of, 309 
"phantom tumor" of, 325 
regions of, 298, 299 
scaphoid, 300 

swelling in epigastrium, 303, 311 
tumors of, 307, 311 

position in, 2 1 
wall inspection of, 308 

protrusion of, 299 

retraction of, 300 
Abscess, cerebral, character of pain in, 

481 
choked disk not generally present in, 

3»7» 459 
coma in, 438 
diagnosis of, 459 
fever in, 459 
gangrene in, 159 

symptoms of, 424, 438 

tache cerebrale a sign of, 144 

vomiting in, 459 
hepatic, brick-dust sputum in, 475 

bulging of abdominal wall, 303 

dysentery a cause of, 407 

fever in, 405 

hiccough in, 455 

pain in, 486 

sweating in, 405 

symptoms and signs of pyemic, 320 
of tropical, 320 

tongue in, 195 

vomiting in, 469 
lumbar, sciatic pain in, 483 
mastoid, edema back of ear in, 165 
mediastinal, acute history in, 258 

cold, 258 

diagnosis of, 258 

purulent sputum in, 475 
of pancreas, 316 
perinephritis 325 



Abscess, pulmonary, chronic morning 
cough in, 472 
copious and purulent sputum in, 

. 2 4 8 > 475 
diagnosis between mediastinal 

growths and, 258 
following amebic dysentery, an- 
chovy-sauce sputum in, 475 
history, signs, and symptoms of, 

248, 249 
rapidity of respiration in, 216 
pyopneumothorax subphrenicus, 323 
retro-esophageal. See Retro-esopha- 

geal abscess, 
subphrenic, purulent sputum in, 475, 
476 
Absolute arrhythmia, 283 
Accommodation, pupillary reaction to, 

374 
"Accoucheur's hand" in tetany, 60, 451 
Acne due to bromine or iodine, 155 
to iron, 156 

to working in paraffin, 156 
of forehead, purulent, in syphilis, 155 
Acromegaly, enlargement of feet in, 101 
of tongue in, 200 
face of , 33 
head in, 46 
spade-like hand in, 55 
Acroparesthesia, 187 

diagnosis of, 187, 188 
Actinomycosis as a cause of empyema, 
252 
enlargement of tongue in, 200 
Acuity of vision, changes in, 377 
Addison's disease, coma in, 433 
convulsions in, 449 
heart in, 277 

pigmentation of buccal mucous 
membrane in, 206, 277 
of skin in, 139, 277 
symptoms of, 139 
tongue in, 196 
Adherent pericardium, reduplication of 
heart sound in, 260 
symptoms of, 220 
Adhesive pericarditis, symptoms of. 

320 
Adiposis dolorosa, 100 
Adults, facial expression in, 29 



5°° 



INDEX 



Agraphia, 128 

location of lesion in, 128 
Ague cake, 326 
Ainhum, 108 

Air passages, foreign bodies in, 256 
"Alar chest" of phthisis, 211 
Albuminuria in acute diffuse nephritis, 
356 

marked, or absent, in amyloid kidney, 

348 

transient, in chronic interstitial 
nephritis, 357 
Albuminuric retinitis, 388 
Alcohol poisoning, tremors in, 63 
Alcoholic epilepsy, 443 
Alcoholism, coma in acute, 433 

convulsions due to, 443 

hyperesthesia in chronic, 189 

morning vomiting in, 456 

symptoms of acute, 437 

tremor of tongue in, 202 
Alexia, 128 

Alkaptonuria, 138, 348 
Allen's test in phthiriasis versicolor, 

J 38 . . 
Allochiria in hysteria, 187 
in multiple sclerosis, 187 
in myelitis, 187 
in paralysis agitans, 187 
in tabes dorsalis, 187 
Amaurosis, 383 
in brain fever, 421 
uremic, 383, 459 
Amaurotic family idiocy, 84 
Amblyopia, 387 
Ameba coli, 335 
Amebic dysentery, 335 
Amphoric breathing in pneumothorax, 
237 
in small cavity, 237 
Amblyopia, tobacco, 387 
• toxic, 387 

Amyloid disease of kidney, hyaline, 
fatty, and granular casts in 
urine in, 348 
of liver, 318 
jaundice in, 135 
Amyotrophic lateral sclerosis, hands in, 

58 
Analgesia in locomotor ataxia, 174 

in Morvan's disease, 58 
Anasarca, general. See General ana- 
sarca. 
Anchovy-sauce sputum, 475 
Anemia, Bothriocephalus latus a cause 
of, 34 2 
cerebral choked disk in, 459 
vertigo in, 432 
vomiting in profound, 459 
dropsy of feet and legs in, 164 
edema in, 163 
headache in, 431 
hiccough in, 455 



Anemia, hyperesthesia in, 190 
in acute diffuse nephritis, 356 
in ankylostomum duodenale, 342 
in gastric ulcer, 313 
in pyelitis, 355 
nails in, 49 
of convalescence, dilatation of pupil 

in, 376 
pallor of conjunctiva in, 359 
papillitis in, 386 

pernicious, chills followed by fever in, 
407 

fatty degeneration of heart in, 

V 6 

indicanuria in, 355 

jaundice in, 136 
pernicious, pulsating cervical vessels 
in, 218 

vertigo in, 432 

purpuric eruptions in, 143 

splenic, 326 

blood changes in, 326 

tongue in, 195 
Anemic heart murmur, 261 

necrosis, 276 
Anesthesia, 170 

bilateral, in chorea, 173 

in Friedreich's ataxia, 176 

in hemorrhage of cord, 175 

in hysteria, 173 

in injuries of cord, 174, 175 

in lesions of pons, 174 

in locomotor ataxia, 174, 175 

in meningitis, spinal, 174 

in myelitis, 174, 175 

in spinal disease, 174 

in syringomyelia, 176 
causes of, 170 
crossed, in lesions of one side of cord, 

173 

of peduncle, 173 
of pons, 173 

differential diagnosis in facial, 
186 

distribution of, in special nerve in- 
volvement, 181, 183 

dolorosa in cancer of spine, 176 

gauntlet or stocking form of, 173 

in hysteria, 170 

in the spinal cord, 175 

neuritis as cause of, 180 

of body and legs in locomotor ataxia, 

174 
of face, 186 

of Friedreich's ataxia, 176 
of myelitis, 174, 175 
of toxic peripheral neuritis, 181 
patches of, in syringomyelia, 176 
reflexes preserved in cerebral, 172 
signs of, due to neuritis, 180 
unilateral, 172 
varieties of, 170 
zones of, 176, 179 



INDEX 



SOI 



Aneurysm, aortic, blood-streaked spu- 
tum due to leakage from aorta 
in, 475 
bruit in, 269 

bulging of chest in, 213, 271 
hemoptysis in, 475 
pain in, 271, 475, 482 
appearance of hands in, 49 
brassy cough due to pressure on 

larynx by, 271, 473 
bruit in, 269 

dyspnea or dysphagia in, 206, 271 
edema of upper extremities in, 165 
enlarged cervical vessels in, 219 
hemorrhagic pleural effusion in, 253 
hoarseness of voice due to pressure 
on recurrent laryngeal nerve by, 
271 
intracranial, headache due to, 431 
laryngeal spasm due to pressure on 
recurrent laryngeal nerve by, 256, 
271 
loss of pulsation in peripheral vessels 

in, 272 
of abdominal aorta, 315 
pain in abdominal, 271, 482, 490 
pressure on bile duct causing jaun- 
dice in, 133 
pupillary contraction in, 271 

dilatation in, 271 
sweating of side of head in, 162 
symptoms of, 270, 271 
thoracic diagnosis of, from medias- 
tinal growths, 257 
pain in, 257 
tracheal tugging in, 272 
Angina, Ludwig's, 205 
Vincent's, 205 
pectoris, causes of, 291 
pain in, 481, 482 
symptoms of, 482 
Angioneurotic edema, eyelids in, 145, 
164 
hands in, 54 
pain in, 487 
skin in, 145 
Ankle clonus, how best elicited, 498 
in amyotrophic lateral sclerosis, 498 
in ataxic paraplegia, 80 
in disseminated sclerosis, 498 
in hysteria, 498 
in lateral sclerosis, 498 
Ankylostomum duodenale, 342 

anemia due to, 342 
Annulus migrans, 199 

senilis, 360 
Anthrax maligna, anthrax bacilli in, 145 
fever in, 145 
symptoms of, 145 
simplex. See Carbuncle. 
Antidiphtheritic serum, roseola due to 

injection of, 148 
Anus, fissure of, diarrhea in, 333 



Anus, fissure of, pain in, 492 
Aorta, aneurysm of abdominal 315 
of descending, symptoms of, 271 
of greater curvature of ascending, 

symptoms of, 271 
of transverse portion of arch of, 
symptoms of, 271 
Aortic aneurysm, bruit in, 269 

diagnosis of, by fluoroscope, 272 
pain in, 482 
pulse in, 269 
regurgitation, 267 
"ox-heart" of, 267 
pulse in, 280 
Quincke's sign of, 267 
"water-hammer" pulse in, 267 
stenosis, 266 
pulse in, 280 
reduplication of heart sounds in, 

260 
symptoms of, 267 
valvular disease, 266 
Aortitis, acute, causes of, 482 

pain in, 482 
Apex beat, 221 

Aphasia, due to hematoma near island 
of Reil, 121 
to hemorrhage into island of Reil, 
121 
Aphemia, 128 

Aphonia due to pressure in aortic an- 
eurysm, 271 
in hysteria, 125 
Aphthongia, spasm of tongue in, 202 
Apoplexy, cause of, 290 

Cheyne-Stokes breathing in, 217, 

437. 
coma in, 437 
conjugate lateral paralysis of ocular 

muscles in, 371 
contractions following, 59 
diagnosis between coma of, and alco- 
holism, 437 
epilepsy associated with, 442 
ingravescent, 119 
knee-jerk decreased after shock, 495 

exaggerated after shock, 496 
paralytic chorea following, 62 
passage of urine in, 346 
skin reflexes lost when deep reflexes 

are exaggerated, 497 
vertigo before, 432 
Appendicitis, fever in, 311 
conditions simulating, 3 1 1 
pain in, 310, 485, 488 
symptoms of, 311, 315 

in groin, 328 
vomiting in, 465 
Apraxia, 128 
Arcus senilis, 276, 360 
Argyll-Robertson pupil, 74. 374 

not present in ataxic paraplegia, 
80 



502 



INDEX 



Argyll-Robertson pupil in Friedreich's : 
ataxia, 78 
in true ataxia, 374 
present in diabetes mellitus rarely, 

74- 374 
Argyria, 137, 139 
Arrhythmia in cardiac dilatation, 275 

absolute, 283 
Arms, spastic rigidity of, sign of chronic 
hydrocephalus of, 60 
tumors of, 63 
Arrested development, cerebral spastic 

paraplegia in, 84 
Arsenical neuritis, 65 
Arterial disease, ophthalmoscopic evi- 
dence of, 389 
sclerosis, heart sounds in, 258 
tension, 286 

causes of, 286, 288 
estimation of, 287 
high, reduplication of heart sounds 
in, 260 
persistent, 290 
in acute diffuse nephritis, 356 

normal, 287 
low, 292 
temporary, 289 
Arteriocapillary fibrosis, high blood 

tension in, 290 
Arteritis, syphilitic, 422 

facial paralysis in, 36 
Artery of cerebral hemorrhage, 118 
Arthralgic form of gonorrheal arthritis, 

102 
Arthritis deformans, fingers in, 51, 52 
Heberden's nodes in, 52 . 
joints in, 102, 103 
knee-jerk increased in, 496 
seal-fin hand of, 52 
gonorrheal, 102 
in acute osteomyelitis, 104 
multiple, in dengue, 105 
of cerebrospinal meningitis, 104 
septic, hands in, 53 
joints in, 104 
Arthropathies, 102 
Ascaris lumbricoides, 342 
Ascites, apex beat raised in, 222, 303 
caput Medusas in hepatic cirrhosis 

causing, 303 
causes of, 303 
diagnosis of, 302 
rapid respiration in, 218 
skin of abdomen in, 303 
Astasia abasia, 82 
Astereognosis, 168 
Asthenic bulbar paralysis, 41 
Asthma, catarrhal pneumonia following, 
256 
character of rales in, 256 
due to cardiac lesions, 256 
to gastric disorders, 256 
to reflex nasal irritation, 256 



Asthma, due to renal disease, 256 
erect position in, 255 
expiration prolonged in, 217, 255 
physical signs and symptoms of, 255 
rapid respiration in, 216 
sputum of, Charcot-Leyden crystals 
in, 477 
Curschmann's spirals in, 477 
pearls of mucus in, 476 
Astigmatism, headache due to, 418 
Asymmetry, facial, 32 
Asynchronism of ventricles, reduplica- 
tion of first sound of heart due to, 
260 
Ataxia, differential diagnosis of, 78 
Friedreich's. See Friedreich's ataxia, 
hereditary cerebellar, 78 

spinal. See Friedreich's ataxia, 
locomotor. See Locomotor ataxia. 
Ataxic paraplegia, 80, 95 
Atheroma, headache in, 419 

in chronic interstitial nephritis, 357 
vertigo in, 432 
Athetosis, 66 

reflexes increased in, 498 
Atrophy, acute yellow, of the liver, 
coma in, 436 
hematemesis in, 467 
jaundice in, 136 
vomiting in, 469 
bilateral, of tongue, causes of, 199 
faciohumeroscapular type of, 31 
idiopathic muscular, ptosis in, 40 
of nails, 50 
optic, 388 

progressive muscular, 57 
claw-hand in, 56 
condition of reflexes in, 497 
fibrillary twitch in, 66 
sweating of hand in, 51 
unilateral, of tongue in chronic lead 
poisoning, 199 
Aura, 440 

Auricular fibrillation, 265, 285 
Auscultation of heart and vessels, 258 

of respiratory apparatus, 235 
Auto-intoxication, headache in, 418 
poisons causing, 418 
symptoms of, 418 



B 



Babinski's reflex, 420, 497 

Baccelli's sign, 241 

Bacilli, in stools in cholera, 332 

in tuberculous pyelitis, 355 

of Eberth, in stools of typhoid fever, 

399 

Bacillus typhosus, cause of empyema, 

252 
Banti's disease, 326 
symptoms of, 326 



INDEX 



503 



Barrel-shaped chest in emphysema, 

212, 254 
Basedow's disease, tremor of hand in, 

65 

Bed-sores in acute transverse myelitis, 
88, 160 

in hemiplegia, 160 

in hemorrhage into spinal cord, 96 

in paretic dementia, 160 

in typhoid fever, 160 
Bergeron's chorea, 62 
Beriberi, general anasarca in, 163 
Biceps, tendon reflex, how developed, 

72 
Bilateral anesthesia, 173 

facial paralysis, 40 

ptosis, 40 

wrist-drop, 61 
Bile ducts, obstruction of, 321 

in urine, test for, 354 
Bilious remittent fever. See Malaria, 

remittent. 
Biliousness, tongue in, 193 
Bismuth, odor of breath after admin- 
istration of, 19 
Black vomit in yellow fever, 408 
Bladder, 343 

causes of incontinence of urine in, 

345 

of retention of urine in, 343 
character of blood in urine from, 

348 
nervous, 346 
paralysis of, 343 
sensory disorders of, 345 
stone in, 346 
symptoms of diseases of, 343 

of inflammation of, 345 

of locomotor ataxia, 344 

of myelitis, 88, 343 

of paretic dementia, 344 

of tabes, 344 
tumors of, obstructing urinary flow, 

346 
Blepharofacial spasm, 43 
Blindness, causes of, 377, 383 
Blood, circulation of, 278 
from kidney, 351 
in sputum, 474 
in stools, 335, 337, 464 

in dysentery, 334, 335 

in enterocolitis, 333 
in urine, 348 

in severe renal disease, 490 
in vomitus, 466, 467 
pressure, estimation of, 287 

high, 289, 290 

Korotkoff's method of, 289 

normal, 287 

low, 292 
streams of retinal, influence of arte- 
rial pressure on, 389 
Bloodvessels and pulse, 278 



Blue line on gums in lead poisoning, 75, 

203 
Boils in diabetes mellitus, 158 
in paraffin- workers, 158 
in tar- workers, 158 
Bothriocephalus latus, 342 
Bowels, cancer of, 316 

constipated, in jaundice, 133 

in obstruction, 330 
sloughs of, in intussusception, 338 
Brachial monoplegia, 66 
apparent, 70 
bilateral, 70 
cortical lesions in, 66 
due to cortical lesions, 66 
to crutch paralysis, 70 
to fracture or dislocation of the 

head of humerus, 69 
to growth in neck or axilla, 69 
to hysteria, 68 
to injury of brachial plexus or 

important branches, 68 
to lead poisoning, 70 
to locomotor ataxia, 69 
to primary brachial neuritis, 68 
Erb's paralysis, 69 
Klumpke's paralysis, 70 
paralysis of special muscles in, 70 
signal symptoms of cortical, 67 
paresthesia, 71 
Bradycardia, 275 
in jaundice, 276 
in some infectious diseases, 276 
Brain abscess, 424 
areas of, 112 
tumors of, anesthesia in, 171 

Cheyne-Stokes breathing in, 218 
convulsions in, 420 
diagnosis of, 422 

differential, between chronic 
nephritis and, 422 
focal symptoms of, 421 
headache in, 420 
hyperesthesia in, 189 
papillitis of optic nerve in, 387, 420 
paralysis in, 421 
paresthesia in, 187 
slow breathing in, 422 

pulse in, 422 
vertigo in, 432 
vomiting in, 420 
Breakbone fever, 147. See Dengue. 
Breast, pigeon, 213 

Breath after the administration of bis- 
muth, 19 
in bronchiectasis, 19, 249 
in chronic atrophic nasal catarrh. 19 
in diabetes mellitus, 19 
in diphtheria, 19 
in empyema opening into bronchus, 

in fever, 19 

in gangrenous stomatitis, 19 



504 



INDEX 



Breath in gastric disorders, 19 
in heart disease, 268, 271, 273 
in ozena, 19 

in pulmonary gangrene, 19, 249 
in tonsillitis, 19 
in uremia, 19 
Breathing, amphoric, 237 
blowing, 237 
bronchial, 236, 237 
bronchovesicular, 236 
cavernous, 237 
cog-wheel, 236 
irregular, 236 
puerile, 236 
tubular, 235, 236 
vesicular, 235, 236 
wavy, 218 
Bright's disease. See also Kidneys and 
Nephritis. 
complications of, 357 
obstinate cough in, 472 
retinal hemorrhage in, 388 
retinitis in, 388 
roseola in, 148, 149 
secondary diphtheritic dysentery 

in, 335 
sputum in, 476 
Brill's disease, 401 
fever in, 401 
eruption in, 401 
Broadbent's sign of adherent pericar- 
dium, 220 
Bromidrosis, cold, clammy hands in, 51 

in hysteria, 162 
Bronchial breathing, 236, 237 

due to compression of lungs over 

pleural effusion, 237 
in catarrhal pneumonia, 237 
in cavity, 237 
in consolidation, 237 
Bronchiectasis, fetid breath of, 19, 249 

sacculated morning cough in, 472 
Bronchitis, acute, sputum in later 
stages of, 474 
bronchorrhea in, 254 
Charcot-Leyden crystals in, 477 
chronic, in chronic interstitial neph- 
ritis, 357 
fever in, 413 
fibrinous, small casts of bronchioles 

coughed up in, 477 
hard, dry cough in, 253, 471 
moderate, early in typhoid fever, 398 

399 

physical signs of, 254 
putrid, 254 

Dittrich's plugs in sputum of, 254 
rales, 254 

bubbling, 238 
rapidity of respiration in severe, 216 
Bronchophony in pleural effusions, 241 

in tuberculosis of lungs, 246 
Bronchovesicular breathing, 236 



Brow T ague in malaria, 431, 479 
"Bruit" in aortic aneurysm, 269 
Bullae due to antipyrine or iodine, 159 

to pemphigus, 158 

to trophic lesions in diseases of 
central nervous system, 158 
Burns, hemoglobinuria after severe, 352 
Bursal gonorrheal arthritis, 103 



Cachexia, anasarca in cancerous, 164 
Calculi, fecal, 338 
Calculus. See also Stone, 
pancreatic, pain in, 486 
renal, pain in, 490 

vomiting in, 469, 490 
salivary, 203 

vesical, symptoms of, 355, 490 
Capillary pulse, 267 
Caput coli, diseases of, 328 
carcinoma of pain in, 485 
Medusae, 303 
Carbuncle, 158 

Carcinoma, bulging of abdominal wall 
in, 303. 
jaundice in, 134 
face in, expression of, 27 

pallor of, 138 
esophageal, brassy cough due to 
pressure on larynx by, 473 
stricture due to, 206 
gastric, anemia in, 312 

character of vomiting in, 466 
coffee-ground vomit in, 312, 466 
fever in, 407 
indicanuria in, 355 
most frequent at pylorus, 312 
hemorrhagic effusion in pleura in, 

2 53 
melanotic, black urine in, 348 
of bowel, 316 
of caput coli, 328 

pain in, 485 
of gall-bladder, 321 
of liver, indicanuria in, 355 
of pancreas, diabetes mellitus in, 315 
of pylorus, diagnosis of, 312 

between gastric ulcer and, 313 
dilatation of spleen, 327 
of stomach due to, 312 
symptoms of, 312 
renal hematuria in, 350 
retraction of abdominal wall in, 309 
skin in, 138 
Cardiac crises, 274 
arrhythmia, 275 
dilatation, 273 
disease in children, pain in, 22 

congenital diagnosis, of 268 
dulness, alterations in, due to valvu- 
lar lesion, 235 



INDEX 



505 



Cardiac dulness, increase of, due to 
hypertrophy or dilatation of 
heart, 231 
due to pericardial effusion, 232 
normal extent of, 229 . 
feebleness, 274 
hypertrophy, 275 

in aortic regurgitation, 267 
triangles, 229, 230 
Cardiopulmonary murmur, 260 
Caries of bones of skull, headache in, 

431 . 
of cervical vertebrae, head in, 45 
of teeth in pregnancy and diabetes 

mellitus, 203 
of vertebras, paraplegia due to, 83 
spinal, symptoms of, 325, 483 
Carphologia, 51, 66 
Carpopedal spasm, in rickety, hydro- 

cephaloid children, 60 
Catalepsy, 30 

Cataract, congenital, nystagmus in, 373 
Catarrh, acute gastric, symptoms of, 
456 
tongue in, 194, 456 
vomiting in, 456 
rectal, symptoms of, 334 
chronic gastric, morning vomiting of 
drunkards in, 456 
vomiting due to excessive tea- 
drinking in, 456 
gastro-intestinal, fever in mild, in 

children, 394 
frog-belly in children with, 300 
laryngeal spasm due to, 256 
nasal, headache due to, 431 

chronic, odor of breath in, 19 
of middle ear in syphilis, 203 
persistence of fever in measles due 
to bronchial or gastro-intestinal, 

4? 2 . -» 

respiratory cough in, 473 

Catarrhal fever. See Influenza, 
jaundice, 133 

pneumonia. See Pneumonia, catar- 
rhal. 
Cavernous breathing, 237 

sinus, thrombosis of, 482 
Cephalalgia. See Headache. 
Cephalic tetanus, 45 
Cerebellar ataxia, hereditary, 78 
disease, gait in, 82 

vomit in, 460 
hemorrhage, 121 
titubation, 82 
Cerebral abscess, coma in, 438 
pain in, 481 
papillitis in, 387 
vomiting in, 459 
effusion, 46 
embolism, brachial monoplegia in, 

6 7 . . 
hemiplegia in, 121 



Cerebral hemorrhage, artery of, 118 
ptosis from, 38 
pupil in, 375 
palsy of children, 59 
athetosis in, 66 

epileptiform convulsions in, 59 
flexion of hands in, 59 
gait in, 79 

intention tremor in, 59 
knee-jerk in, 496 
softening, coma of, 438 

symptoms of, 438 
spastic paraplegia, 83, 84 
syphilis, coma in, 439 

hemiplegia in, 122 
thrombosis, edema in, 165 

hemiplegia in, 121 
tumor, pain in, 481 

spastic hemiplegia in, 122 
vomiting in, 459 
Cerebrospinal fever, Cheyne-Stokes 
respiration in, 217 
character of fever in, 410 
convulsions in, 410 
diagnosis between croupous pneu- 
monia, otitis media, tubercu- 
lous infection, and, 410, 411 
lumbar puncture in, 410 
epidemic, coma in, 439 
headache in, 410 
herpes labialis in, 158 
hyperesthesia in, 189 
joints in, 102, 104 
meningitis, 409 
petechias in, 143 
retraction of head in, 45, 410 
meningitis, rigidity of back of neck 
in, 410 
vomiting in, 410 
sclerosis, multiple, 85 
Cestodes, 338 
Chancre of tongue, 197 
Charcot-Leyden crystals in acute bron- 
chitis, 477 
in asthmatic attacks, 477 
in chronic croupous pneumonia, 

477- 
in pulmonary tuberculosis, 477 
Charcot's fever, 134, 405 
Cheek, swelling of, in noma, 203 
in salivary calculus, 203 
in Schonlein's disease, 203 
in stomatitis, 203 
Chest, auscultation of, 235 

barrel-shaped, of emphysema, 212 
beaded ribs of, in rickets, 213, 215 
bulging of, causes of, 212 

of sternum in pigeon breast, 213 
expansion, 218 
friction sounds in, 231) 
Harrison's grooves in, 213 
inspection of abnormal, 212 
of normal, 208 



;o6 



INDEX 



Chest, localized bulging of, 213, 219 
pain in, in children, 27 
palpation of, 220 
percussion of, 223 
phthisical or alar, 212 
resonance of, 224 
shrinking of, 215 
tumors of, 257 

variation in shape of, in health, 211 
wall, pulsations on, causes of, 219 
Cheyne-Stokes respiration, causes of, 
218 
prognostic value of, 218 
pupillary reaction associated with, 

377 
Chicken-pox, eruption in, 154, 157 
fever in, 403 

disparity between height of, and 
degree of illness in, 403 
Children, examination of, 22 
Chill in acute pleurisy, 249 
in croupous pneumonia, 412 
in dysentery, 334 
in intermittent malarial fever, 403 
in pernicious anemia, 407 
in pyelitis, 355, 407 
in septic poisoning, 407 
Chills, 390 
Chilly sensations and nausea in acute 

diffuse nephritis, 356 
Chin-jerk, how elicited, 494 

position of, wryneck, 44 
Chlorosis, greenish-yellow color in, 138 

pallor of, 26, 139 
Choked disk, 386 

in cerebellar tumor, 386, 459 
- in cerebral anemia, 459 
tumor, 386, 459 
Cholangitis, catarrhal or suppurative, 
fever in, 322, 405 
gall-stone colic in, 407 
jaundice in, 407 
leukocytosis in, 407 
Cholecystitis, acute, pain in, 316, 485, 

486 
Cholelithiasis, 486 
Cholera Asiatica, comma bacillus in, 

33i 

diagnosis of, 330, 331 

Hippocratic face in impending 
death in, 31 

indicanuria in, 355 

roseola in, 147, 148 

skin in, 162 

subnormal temperature in, 415 

systemic infection in, 331 

temperature in, 331 

vomiting in, 331, 465 
infantum, fever in, 331 
odor of stools in, 337 

Cheyne-Stokes respiration in, 331 

cold skin and high rectal tempera- 
ture in, 331 



Cholera infantum, diarrhea in. 331 

disparity between axillary and 

rectal temperature, 331 
sinking in of fontanelles in, 47 
subnormal temperature in, 415 
symptoms of, 331 
vomiting in, 331, 465, 466 
morbus, subnormal temperature in, 

415 
symptoms of, 330 
nostras. See Cholera morbus. 
Chorea, anemic murmurs in children in, 
261 
anesthesia in, 170 
Bergeron's 62 

character of spasms in, 451, 452 
diagnosis of, 452 
electric, 62, 453 
expression in, 30 
facial spasm in, 42 
habit, 62 

heart disease in, 261 
hereditary, 63 
Huntingdon's, 63, 452 
hysterical, 62 
insaniens, 452 
loss of knee-jerk in, 495 
major, 453 
maniacal, 62 

minor, movements in, 61, 62, 451 
nodding spasm in, 44 
paralytic, 62 

postemiplegic lesion of, 121 
senile, 62 

spasm of face in, 42 
of tongue in, 202 
Choroid, tubercle of, 426 
Chromophytosis, skin in, 138 
Chvostek's symptom of tetany, 451 
Chyluria, caused by Filaria sanguinis 

hominis, 352, 355 
Cirrhosis, hepatic ascites in, 164, 318 
caput Medusa? in, 303 
disorders of digestion in, 319 
enlargement of spleen in, 326 
hematemesis in, 319, 467 
jaundice in, 134 
symptoms due to, 319 
Claw-foot, 101 

in Friedreich's ataxia, 101 
Claw-hand, 55 

Clothing, diagnostic significance of, 18 
Clubbed fingers, 49 

Coffee-ground vomit in gastric cancer, 
466 
in locomotor ataxia, 467 
in phosphorus poisoning, 468 
Cog-wheel breathing, 236 
Coin percussion in pleural effusion with 

pneumothorax, 252 
Cold abscess of mediastinum, 258 
Colic, abdominal, 485 
in children, 23 



INDEX 



507 



Colic due to Strongylus gigas, 352 
gall-stone, in catarrhal cholangitis, 

321, 407 
hepatic, 133, 485 
lead, pain in, 489 
renal, pain in, 490 
diagnosis of, 490 
retraction of abdominal wall in re- 
nal, hepatic, and lead, 300 
Collapse, profuse sweating a sign of, 162 
of lung, tympanitic percussion sound 
in, 227 
"Collar of brawn" in scarlet fever, 402 
Colon bacillus as a cause of empyema, 

2 5 2 
Coma, ability to protrude tongue in, 
when other orders fail to gain 
response, 200 
causes of, 433 
following pernicious malarial fever, 

437 
position in, 20 
in acute alcoholic poisoning, 433 

differential diagnosis of. 434, 

435 

yellow atrophy of liver, 436 
in Addison's disease, 433 
in apoplexy, 437 
in cannabis indica poisoning, 435 
in cerebral abscess, 438 

disease, 20 

softening, 438 

syphilis, 439 
in chloral poisoning, 435 
in chronic parenchymatous nephritis, 

357 
in cirrhosis of liver, 319 
in diabetes, 357, 436 
in epidemic cerebrospinal meningitis, 

439 

in epilepsy, 439 

in general paralysis, 439 

in heart failure, 433 

in heart-stroke, 439 

in multiple sclerosis, 439 

in opium poisoning, 434 

in pernicious malarial infection, 437 

in petit mal, 439 

in purulent leptomeningitis, 438 

in Raynaud's disease, 438 

in renal disease, 20, 21 

in subdural hemorrhage, 438 

in thrombosis of brain sinuses, 438 

in typhoid fever, 436 

in uremia, 436 

rapidity of respiration in diabetic or 
uremic, 217, 436 

slowness of breathing in uremic or 
diabetic, 217, 436 

vigil, 436 
Concomitant squint, 362 
Congenital asymmetry of face, 32 

cardiac disease, diagnosis of, 272 



Congenital cataract, nystagmus in, 373 

lymphangioma, tongue in, 199 

malformations of heart, 268 
rules for diagnosis of, 268 

ptosis with facial paralysis, 38 
Congestion, hepatic tenderness in, 319 

pulmonary, 249 
Conjugate lateral ocular paralysis, 371 
Consensual pupillary reflex to light, 374 
Constipation, causes of, 329 

in chronic lead poisoning, 330 

in diabetes insipidus, 329 
mellitus, 329 

in hepatic disease, 329 

in intestinal obstruction, 330, 46o ; 

463 
in jaundice, 329 
in pelvic disorders, 330 
in phosphorus poisoning, 329 
in reflex irritation, 330 
indicanuria in, 355 
Continued fever. See Malaria, remit- 
tent. 
Contraction of pupil of eye, 374 
Contractures in hysteria, 60, 87 

in cerebral spastic paraplegia, 84 
Convulsions or general spasms, 440 

in acute articular rheumatism 

with hyperpyrexia, 414 
in Addison's disease, 449 
in anterior poliomyelitis, 95 
in brain tumor, 421 
in cerebrospinal meningitis, 410 
in uremia, 445, 448 
clonic, at onset of apoplexy, 442 
in acute alcoholism, 443 
in cerebral spastic paraplegia, 84 
in chronic lead poisoning, 444 
in epilepsy, 440 
in general paresis, 77 
in hysteria, 445, 446, 447 
in irrigation of pleural cavity, 449 
in Jacksonian epilepsy, 441 
in malingerers, 449 
in multiple sclerosis, 449 
in posthemiplegic epilepsy, 442 
in puerperal eclampsia, 448 
in syncope, 449 
in syphilitic epilepsy, 443 
epileptiform, in cerebral palsy of 

children, 59 
erotic, in phosphorus poisoning, 468 
of infants in meningitis, 450 
in pseudomeningitis, 450 
in reflex irritation, 450 
salaam, 453 

tetanic, in strychnine poisoning, 450 
in tetanus, 450 
in tetany, 451 
Convulsive tic, 63 

facial spasm in, 4.2 
Coprolalia, 43, 63 
Coproliths, 338 



5 o8 



INDEX 



Corrigan's pulse, 267, 279 
Coryza, action of child toward breast 
in, 23 
in influenza, 412 
Cough and expectoration, 471 
causes of night, 473 
chronic loose, in empyema, rupturing 
into bronchus, 472 
in pulmonary abscess, 472 
in sacculated bronchiectasis, 472 
in tuberculosis with cavity, 472 
dry and hacking, in phthisis pulmo- 
nalis, acute bronchitis, and pneu- 
monia before exudation, 471 
due to change of position in pleurisy 

with effusion, 473 
during aspiration of fluid in pleurisy, 

473 
followed by cry in pneumonia or 

pleurisy, in children, 23 
hard and dry, in acute bronchitis, 253, 

.471 

in acute laryngitis, 473 

in aneurysm of transverse arch of 
aorta, 271 

in false croup, 471, 473 

in laryngeal phthisis, 473 

in whooping-cough, 471 

laryngeal, due to irritant dust or 
vapors, 471, 473 
to mediastinal tumors, 473 
to pressure by aneurysm, 473 

by carcinoma of esophagus, 

473 „ 

nervous or reflex, 472 

obstinate, in Bright's disease, 472 
larged uvula, hypertrophy of mu- 
coud membrane of the nose, etc., 

.473 

significance of cessation of, in ad- 
vanced phthisis, bronchorrhea of 
old and severe pneumonia, 474 
smothered or suppressed, in pleuro- 

pulmonary inflammation, 472 
value of loose, 472 
varieties of, 47 1 
Courvoisier's law, 322 
Coxalgia, pain in, 22, 483, 484 
Cracked-pot sound, 228 
Craniotabes, 46 
Cremasteric reflex, in, 494 
Crepitant rales, 238 
Cretinism, facial expression in, 31 

shape of head in, 46 
Crisis, apparent, in relapsing fever, 
401 
fever in erysipelas ending by either 

lysis or, 403 
gastric, in locomotor ataxia, 74, 467 
in croupous pneumonia, 412 
in typhus fever, 400 
intestinal, 332 
subnormal temperature at, 415 



Crisis with fading of eruption in 

measles, 402 
Croup, spasmodic, cough in, 471, 473 
inspirations prolonged in, 217 
laryngeal spasm in, 256 
Croupous pneumonia. See Pneumonia, 

croupous. 
Crutch palsy, 61 
Crying in children, 23 
Crystals, Charcot- Ley den, 477 
Curschmann's spirals in asthmatic 
attacks, 477 
in croupous pneumonia, 477 
in pulmonary tuberculosis, 477 
Curvature of spine, bulging of chest in, 

213 
Cyanosis, causes of, 140 
due to drugs, 140 

in acute articular rheumatism with 
hyperpyrexia, 414 
miliary tuberculosis, 411 
in cardiac dyspnea, 26 
in laryngeal obstruction, 140 
in newborn, 140 
in pulmonary diseases, 140 
in serious cardiac disease, 140 
Cyclical vomiting, 467 
Cyst, echinococcus, of kidney, 324 
hematuria in renal, 351 
hydatid, of liver, 320 

of spleen, 327 
of kidney, 324 
of mesentery, 325 
of pancreas, 316 
ovarian, diagnosis of, 300 
Cystic degeneration of kidney, 324 
Cystitis, acute, hematuria due to, 351 
color of urine in, 348 
pain in, 492 

in urethra in, 345 
purulent, septic fever in, 343 
tenesmus in, 345 



Dactylitis, 50 

syphilitica in infants, 50 
Deafness, chronic, position of head in, 

45 
Deformity of feet and legs, 101 

in acute cerebral paralysis of 
infancy, 100 
Degenerative myocarditis, 277 
Delirium, in acute articular rheuma- 
tism with hyperpyrexia, 414 
yellow atrophy of liver, 436 
in croupous pneumonia, 243 
in thrombosis of cerebral sinuses, 428 
incoherent speech in, 127 
low, muttering, in typhoid fever, 29, 

399 

mild, in mitral regurgitation, 431 






INDEX 



509 



Delirium, wild, in phosphorus poison- 
ing and in some cases of uremia, 468 
Dementia, paretic, Argyll-Robertson 
pupil in, 374 
diplopia in, 361 
gangrenein, 159 
hemiplegia in, 122 
hemorrhage into skin in, 143 
hesitating, halting speech in, 127 
knee-jerk in, 496 
localized sweating in, 162 
optic atrophy in, 388 
perforating ulcer of foot in, 160 
tache cerebrale in, 144 
tremor of tongue in, 127 
Dengue, 408 

differential diagnosis of, 408, 409 
erythema in, 147 
fever in, 408 
hematemesis in, 467 
jaundice in, 136 
joint involvements in, 105 
pain in, 493 
Dentition, fever in, 394 
Dermatitis, acute exfoliating, 148 
Diabete bronze, 136 
Diabetes insipidus, constipation in, 329 
increase of urine in, 348 
loss of knee-jerk in, 495 
mellitus, Aryll-Robertson pupil in, 

74. 374 

boils in, 158 

breath in, 19 

caries of teeth in, 203 

cataract in, 359 

Cheyne-Stokes respiration in, 218 

coma in, 435 
diagnosis of, 436 

constipation in, 329 

development of, in carcinoma of 
pancreas, 315 

dry, harsh skin in, 162, 163 

furunculosis in, 358 ■ 

gangrene in, 160 
of toes in, 106 

headache rarely in, 420 

jaundice in, 135 

knee-jerk lost in advanced, 495 

ocular palsy in, 368 

paraplegia rare in, 98 
perforating ulcer of foot in, 106 
pruritus in, 190, 357 

color of, 358 

increase of, 347 

odor of, 348 

retinitis in, 388 

roseola in, caused by urine, 150 

specific gravity of, 358 

urine in, 347, 358 
vomiting rare in, 459 

wasting, of hands in, 55 

white spots on trousers in. 18 
Diarrhea, causes of, 330 



Diarrhea, colliquative, in uremia, 459 
decrease of urine due to, 348 
dissecting room, 336 
due to heat prostration, 332 
fatty, due to cod-liver oil, 336 
to disease of pancreas, 336 
in jaundice, 336 
in abdominal pain, 22 
in acute antimony poisoning, 332 
in arsenic poisoning, 332 
in cholera Asiatica, 33 1 
infantum, 331 
morbus, 330 
in dysentery, 334 
in enterocolitis, 333 
in fissure of anus, 333 
in hysteria, 336 
in influenza, 412 
in locomotor ataxia, 332 
in malignant ulceration, 335 
in pellagra, 150 
in proctitis, 334 

in pulmonary gangrene or tuberculo- 
sis, 336 
in renal disease, 332 
in septicemia, 336 
in syphilitic ulceration, 335 
in tuberculosis, 334 
lienteric, 333 

may be caused by purgatives, 22 
nervous, 332 
pain in, 22 
paroxysmal, seromucous or bloody, 

in exophthalmic goitre, 336 
summer, retraction of belly- wall in, 
300 
Diastolic blood-pressure, 287, 289 
Dicrotic pulse, 281 
Dietl's crises, 324 

Digestive disturbances cause of head- 
ache, 416 
of laryngeal spasm, 256 
Dilatation of heart, symptoms and 
physical signs of, 231, 2JT, 
of pupil of eye, 360, 375 
of stomach, 304 

absence of hydrochloric acid in, 

457 

atrophy of gastric tubules in, 

3°6 [ 
constitution of vomitus in, 457 
examination of, 305, 306, 307 
in pressure by growths of pan- 
creas, 457 
in tetany, 60 
Sarcinae ventriculi in, 457 
Torula cerevisia?, 457 
vomiting in, 457 
.v-rays in diagnosis of, 300 
Diphtheria, anesthesia in, 181 
breath in, 19 

casts of larynx and upper bronchial 
lubes at times coughed up in. 477 



S™ 



INDEX 



Diphtheria, difficult swallowing due to 
paralysis from, 206 
double oculomotor paralysis in, 369 
involuntary passage of urine in, 346 
nasal, 205 

paralysis of tongue following, 201 
paraplegia a sequel to, 97 
roseola in, 148 

sickening sweet odor of breath in, 19 
symptoms of, 205, 206 
Diphtheritic dysentery, secondary, 335 

paralysis, dysphagia due to, 206 
Diplegia, spastic congenital, 84 
Diplopia, 360 
crossed, 364 
homonymous, 364 
in meningitis, 361 
in poisoning, 361 
in tuberculosis, 361 
symptoms of Freidreich's ataxia, 361 
of lesion at base of brain, 361 
of cerebral cortex, 361 
of cranial nerve nuclei, 361 
of nerve in its course, 361 
of locomotor ataxia, 361 
of paretic dementia, 361 
vertical, 364 
Disk, optic, 385 
Dislocation, spontaneous, of the hip, 

following infectious diseases, 106 
Dissecting glossitis, 196 

-room diarrhea, 336 
Disseminated sclerosis, facial expres- 
sion in, 30 
hippus in, 376 
nystagmus in, 372 
optic atrophy in, 388 
vertigo in, 432 
Distoma hematobium, hematuria due 

to, 352 
Dittrich's plugs, 254 
Diverticulum of esophagus, 207 
Drop beat, cardiac, 281 
Dropsy, 163. See Edema and General 
anasarca, 
general, in arsenic poisoning, 164 
in beriberi, 163 
in blood diseases, 163 
in cancerous cachexia, 164 
in disordered nervous control of 

vessels, 163 
in emboli, 163 
in heart disease, 163 
in multiple neuritis, 163 
in renal disease, 163 
in scurvy, 164 
in thrombi, 163 
in vascular disease, 163 
localized, in anemia, 164 
in aneurysm, 165 
in angioneurotic edema, 164 
in arsenic poisoning, 164 
in cardiac failure, 164 



Dropsy, localized, in cerebral throm- 
bosis, 165 
in hepatitis or cirrhosis, 164 
in mastoid abscess, 165 
in neuralgia, 165 

in occupations requiring a stand- 
ing position, 164 
in phlegmasia alba dolens, 164 
in pressure on great vein, 164 
in pyothorax, 165 
of eyelids, 164, 165 
of feet and legs in abdominal 
growths, 164 
in anemia, 164 
in cancer of pancreas, 164 
in renal disease, 164 
in scurvy, 164 
in renal disease, 164 
in thrombosis,. 164, 165 
in typhoid fever, 165 
Dry rales, 238 
Dubini's chorea, 62, 453 
Dudgeon's sphygmograph, 281 
Duodenal ulcer, 313 
Dupuytren's contractions, 52 
Dura, hematoma of, 430 
Dynamometer, 72 

Dysentery, acute primary, of a diphthe- 
ritic character, 335 
amebic, Ameba coli cause of, 335 
liver abscess in, 335. 
symptoms of, 335 
arthritis in, 104 

epidemic, due to Shiga's bacillus, 335 
fever in, 334 

secondary diphtheritic, in acute 
croupous pneumonia, 335 
in chronic heart disease, 335 
of Bright 's disease, 335 
slight chill in, 334 
stools in, 334 
thirst in, 334 
tongue in, 195 
tropical, 334 
vomiting in, 466 
Dysmenorrhea, pain in, 492 
Dysphagia, causes of, 206 
due to growths, 206 

stricture, 206 
in aortic aneurysm, 271 
in diphtheritic paralysis, 206 
in glossolabiopharyngeal paralysis, 

206 
in pharyngitis, 206 
in tonsillitis, 206 
Dyspnea from foreign body in air pas- 
sages, 256 
in aortic insufficiency, 268 
in asthma, 256 

in chronic interstitial nephritis, 357 
in heart disease, 29 
in laryngeal spasms, 256 
in miliary tuberculosis, 460 



INDEX 



511 



Dyspnea in pneumothorax, 253 
inspection of chest in, 218 
position due to, 20 



E 



Earache, character of crying in chil- 
dren with, 23 
rubbing of hand over affected side of 
head in, 23 
Echinococcus cysts of kidney, 324 

of liver, jaundice in, 135 
Echolalia, 43, 63 
Eclampsia, puerperal. See Puerperal 

eclampsia. 
Eczema, appearance of nails in, 50 
due to chloral, 158 
to mercury, 158 
to potassium iodide, 158 
to quinine, 158 
Edema. See also Dropsy and General 
anasarca, 
localized, 164 

in thrombosis of cavernous sinus, 428 
of retina in general arterial disease, 

389 

of tongue, 199 

pulmonary, absence of fever in, 249 
crepitant and bubbling rales in, 

238 
due to disease of lungs, 249 

to injury of vagus, 249 
dulness on percussion in, 249 
feeble, hesitating speech in, 126 
in chronic interstitial nephritis, 

357 
position in, 21 
sputum in, 249 

liquid, watery, 476 
Effusion, pericardial, bulging of chest 
wall in, 213 
physical signs of, 231 
pleural, bronchial breathing in, 237, 

251 

accompanied by pneumothorax, 

physical signs of, 250 
bulging of chest- wall in, 212, 213 
decreased vocal fremitus in, 221 

resonance in, 241 
displaced apex beat in, 221, 222 
egophony in, 251 
flat percussion note over effusion, 

228, 249 
Grocco's sign in, 251 
hemorrhagic, 253 
physical signs of, 249, 250, 251 
thrombosis of vena azygos cause of, 

251 

skodaic resonance in, 227, 250 
Egophony, 242 

in pleural effusion, 251 
Elbow-jerk, 72 



Electiic chorea, 62, 453 

Bergeron's, 62 
Embolism, cerebral, brachial monople- 
gia in, 67 
Cheyne-Stokes respiration in, 217 
gangrene in, 93 
hemiplegia in, 12 1, 122 
vomiting in, 459 
of coronary arteries, 275 
edema in, 163 
hematuria in, 349 
of pons Varolii, 414 
Emphysema, barrel-shaped chest of, 
212, 254 
cardiac dulness in, 231, 255 
distended cervical vessels in, 218 
expiration prolonged in, 217, 254 
hands in, 49 

percussion resonance in, 254 
position in, 20 

pulmonary and cardiac hypertrophy 
causing depression of apex beat in, 
221 
rales in, 255 

spleen and liver displaced in, 255, 327 
systolic tricuspid murmur in, 255 
vocal fremitus in, 254 
reasonance in, 241, 254 
Emprosthotonos in hysteria, 446 
Empyema communicating with bron- 
chus, loose morning cough in, 472 
in children, 252 
odor of breath in, 19 
organisms causing, 252 
pulsation of chest wall in, 223 
purulent sputum in, 475, 476 
symptoms of, 252 
Encephalomyelitis, 79 
Endarteritis, syphilitic, immobility of 

pupil in, 375 
Endocarditis, acute ulcerative, chill in 

.390 

diagnosis between typhoid fever 

and, 399 
duration of, 405 
fever in, 399, 405 
hematuria in, 349 
jaundice in, 137 
prognosis of, 405 
purpuric eruptions in, 143 
retinal hemorrhage in, 389 
sweating in, 162 
Enteric fever. See Typhoid fever. 
Enterocolitis, mild follicular, 334 
mucus in stools of, 333 
ribbon-shaped stools in, ^t, 
symptoms of, 333, 334 
ulcerative, 336 
Enteroliths, 338 
Enteroptosis, pain in, 483 
Epidemic cerebrospinal meningitis, 
coma in, 430 
dysentery due to Shiga's bacillus. 335 



512 



INDEX 



Epigastrium, distention of, 303, 311 

pulsation in region of, 220, 315 
Epilepsy, alcoholic, 443 
aura in, 440 

biting of tongue in, 198, 441 
caused by drugs, 444 

by lead, 444 
coma in, 433 
convulsions in, 440 
cutaneous hemorrhage in, 143 
diagnosis between attacks simulated, 
by malingerers and, 449 
hysteria and, 445-447 
puerperal eclampsia and, 448 
syncope and, 449 
uremia and, 445, 448 
expression of face in, 440, 441 
facial spasm in, 42, 440 
fever after seizure of, 448 
hippus in, 376 
idiopathic, 443 

Jacksonian convulsions in, 441, 442 
knee-jerk in, 495, 496 
lead, 444 
malarial, 445 

minor, diagnosis of, 448, 449 
unconsciousness in, 433, 439 
vertigo in, 432 
muscae volitantes in, 383 
myosia at beginning of attack, 375 
nocturnal headache due to, 431 
nystagmus a rare symptom of, 373 
posthemiplegic, 442 
scars on head in suspected traumatic, 

161 
syphilitic, 443 
diagnosis of, 443 
symptoms of, 443 
tache cerebrale in, 144 
vertigo a premonitory symptom of, 
432 
Epileptiform convulsions from cerebral 
hemorrhage, 442 
from other causes, 442 
in cerebral palsy of children, 59 
Epiphysitis of infancy, 105 
Epithelioma ulceration of tongue in, 

197 
Equina. See Glanders. 
Erb's paralysis, 69 

symptom, 451 
Ergotism, gangrene in, 54, 159 

petechias in, 143 
Eruption, date of, in various diseases, 

i I54 

from quinine, 157 

herpetic, in sciatic neuritis, 484 

in anthrax maligna, 145 

simplex, 158 

in Brill's disease, 401 

in chickenpox, 154, 157 

in erysipelas, 144, 145 

in glanders, 145 



Eruption in impetigo contagiosa, 157 
in measles, 153, 402 
in rheumatism, 142 
in rotheln, 152 
in smallpox, 154, 402 
in syphilis, 149 
in typhus, 149, 400 
in vaccinia, 156 
of skin, 141 
pemphigus-like, due to salicylic acid 

or copaiba, 159 
pharyngeal and buccal, in measles, 

153 . 

purpuric, from diseases, 142 
from drugs, 143 

vesicular, about mouth, in foot-and- 
mouth disease in man, 199 
Erysipelas, chill in, 390 

edema of face in, 30 

eruption in, 144 

fever in, 403 

inflammation of skin similar to, from 
arnica, 151 

symptoms of, 144 

vomiting in, 470 
Erythema. See also Roseola. 

by drugs, 147, 150, 151 

exudativum multiforme, 144 

following operation, 147 
parturition, 147 
vaccination, 146 

in Bright's disease, 148, 149 

in cholera, 147, 148 

in dengue, 147 

in diabetes mellitus, 357 

in diphtheria, 148 

in German measles, 152 

in malaria, 148 

in measles, 153 

in pellagra, 150 

in rheumatism, 141 

in rotheln, 152 

in scarlet fever, 146 

in septicemia, 143 

in smallpox, 154, 155 

in syphilis, 148 

in typhoid fever, 149 

roseola, symptoms of, 147 

scarlatiniform, symptoms of, 148 
Escherich's pseudotetanus, 451 
Esophagus, cancer of, 207 

diverticulum of, 207 

hysterical spasm of, 207 

spasmodic contraction of, 206 

stricture of, 206, 207 
diagnosis of, 206 
dysphagia due to, 206, 207 
Esophoria, 362 
Esthesiometer, 167 
Exanthemata, date of eruption of 

various, 154 
Exhaustion from hiccough, 455 
Exophoria, 362 



INDEX 



5 J 3 



Exophthalmic goitre. See Goitre, 

exophthalmic. 
Exophthalmos in thrombosis of caver- 
nous sinus, 428 
Expectoration. See Sputum. 
Expression of face as an aid in diag- 
nosis,' 19 
as an early symptom of facio- 
humeroscapular type of muscu- 
lar atrophy, 31 
elated, of paretic dementia, 30 
excited, of acute mania, 30 
fatuous, of hysteria, 30 
fixed, of catalepsy, 30 
how formed, 25 
how modified, 25 
in acute croupous pneumonia, 27 
fever, 29 
peritonitis, 29 
pulmonary phthisis, 29, 31 
in adults, 29 
in alcoholics, 26 
in children, 27 
in cretinism, 31 
in croupous pneumonia, 27, 29 
in dyspnea of heart disease, 29 
in epileptic seizures, 440, 441 
in Friedreich's ataxia, 31 
in healthy sleeping child, 27 
in hysteria, 30 
in malignant disease, 27 
in melancholia, 30 
in moderate pain in children, 27 
in myxedema, 32 
in nervous exhaustion, 30 
in paralysis agitans, 30 
in peritonitis, 27 
in renal disease, 30 
in typhoid fever, 29 
intellectual, 25 

of anxiety in grave disease, 27 
of "mouth breathers," 29 
variations in, 26 
External squint, causes of, 368 
Extra-systoles, 281 
Eye, alteration of color field of, 382 
amaurosis, 383 
annulus senilis, 360 
arcus senilis, 360 

conjunctival hemorrhage from 
coughing, 359 

coughing, 359 
from degenerative vascular 

changes, 359 
from injury, 359 
diagnosis between ocular symptoms 

of tabes and hysteria, 383 
diplopia, 360 
during menstruation, 26 
examination of, ophthalmoscopic, 

384 
exophthalmos in goitre, 359 

in lesion of oculomotor nerve, 38 

33 



Eye, functional activity of muscles of, 
362 
Graefe's symptom, 359 
hemianopsia, 378 
homonymous and crossed diplopia, 

.363 

in cerebral facial paralysis, 35 
in locomotor ataxia, 388 
intra-ocular muscles of, 373 
muscae volitantes, 383 
orthophoria, 363 
papillitis, 386 
paralysis of, 365, 366 

muscles of, 362 
causes of, 366-368 
pufnness about, from arsenic, 26, 359 

in acute diffuse nephritis, 356 
retinitis, 388 
retrobulbar neuritis, 387 
rod test of Maddox, 363 
squint, 362 

-strain, headache due to, 418 
Eyelids, edematous, in angioneurotic 
edema 145, 164 

from arsenic, 164 

in cerebral thrombosis, 165 

in neurotics, 165 
in healthy sleeping chiid, 27 
painful twitchings of, accompanying 

facial hemiatrophy, 32 
pallor of, in anemia, 359 
pigmentation of, in pregnancy, 26 
puffy, in cardiac disease, 359 

in overuse of arsenic, 359 

in renal disease, 26, 359 

in trichinosis, 30 
slightly parted in sleeping child, 

showing congestive or nervous 

pain, 26 
swollen, in cretinism, 31 

in trichinasis, 30 
twitching in nervous irritation, 27 



Face. See also Expression, 
and head, 25 
anesthesia of, diagnosis of, 186 

due to involvement of the fifth 
nerve or its nucleus, 186 
asymmetry of, congenital, 32 
blurring of features of, in children 

with lesions of mitral valve, 29 
edema of, in dropsy, 30, 163 

in erysipelas, 30 
expression of, 25 

in adults, 29 

in children, 27 

an aid in diagnosis, 19 
faciohumeroscapular type of mus- 
cular atrophy. 31 
full-moon, of myxedema, 32, ^^ 



514 



INDEX 



Face, gray or bluish, from overdose of 

coal-tar products, 26 
heavy, cheesy-looking, in children, 

28 
hemiatrophy of , 32 
hemihypertrophy of, 33 
Hippocratic, of impending death, 31, 

331 

in cholera morbus, 331 
hysterical, 26, 30, 447 
in acute diffuse nephritis, 356 
in angina pectoris, 482 
intellectual, 25 
leonine, of leprosy, 32 
massive, of acromegaly, 33 
of acute peritonitis, 29 
of carcinoma, 27 
of catalepsy, 30 
of cholera, 31 
of chorea in children, 30 
of chronic or subacute renal disease, 

30 
of congenital syphilis, 28 
cretinism, 31 

of disseminated sclerosis, 30 
of exhausting disease, 30 
of Friedreich's ataxia, 31 
of leprosy, 32 
of paralysis agitans, 30 
of pneumonia, severe, 29 
of rickets, 28 
of those exposed to weather, 25 

living indoors, 26 

using alcohol in excess, 26 
of typhoid fever, 29 
pallor of, in chlorosis, 26 

in fright, 26 

in hemorrhage, 26 
paralysis of, bilateral, 40 

unilateral, 34 
parchment-like skin of, in syphilis 

and alcoholic hepatic cirrhosis, 26 
pellucid, in renal disease in children, 

30 
spasm of, 42 
spirituelle, 28 

triangular, in osteitis deformans, 33 
Facial deformity, 32 

expression from nasal obstruction, 29 

in adults, 29 

in children, 27 
paralysis, bilateral, 40 

unilateral, 34 
spasm, 42 
Family idiocy, amaurotic, 84 

periodic paralysis, 98 
Fat, masses of. See Adiposis dolorosa. 
Fatty degeneration in phosphorus 

poisoning, 468 
diarrhea, 336 
heart, 276 
Fecal calculi, 338 
Feces. See also Stools. 



Feces, color of, 337 

consistency of, 336 

impaction of, 316 
pain in, 489 

odor of, 337 

variation in quantity of, 336 
Feet and legs, deformities of, 101 

physical methods in examining, 108 

claw-, 1 01 

contractures of, in hysteria, 60 

deformity of, due to acute cerebral 
paralysis of infancy, 100 
to poliomyelitis, 99 

distribution of anesthesia of, in neu- 
ritis, 184 

enlarged, due to deformity, 102 
in acromegaly, 101 
in myxedema, 102 
in pulmonary osteo-arthropathy, 
101 

flat-, in locomotor ataxia, 102 

numbness of, in locomotor ataxia, 74 

perforating ulcer of, in diabetes, 106 
in senile gangrene, 106 
in tabes dorsalis, 106 

sciopedy, 102 

tabetic, 102 
Femur, malignant growth of, diagnosis 

of, from sciatica, 484, 485 
Fenwick's triangle, 268 
Festination, 82, 452 
Fever, 390 

abscence of, in pulmonary edema, 249 

Charcot's, 134, 405 

cold, wet skin of evil import in, 393 

dry, hot skin in, 393 

flushed face in, 29, 393 

in acute appendicitis, 311 

in anthrax, 145 

in articular rheumatism, 414 

in Brill's disease, 401 

in bronchitis, 413 

in catarrhal pneumonia, 413 

in cerebral abscess, 459 

in cerebrospinal meningitis, 409, 410 

in chicken-pox, 403 

in children, 393 

in cholangitis, catarrhal or sup- 
purative, 322, 407 

in cholera Asiatica, 331 
infantum, 331 

in croupous pneumonia, 412 

in dengue, 408 

in difficult dentition, 394 

in dysentery, 334 

in epilepsy, 448 

in erysipelas, 403 

in foot-and-mouth disease, 199 

in hemoglobinuria, 469 

in hay fever, 412 

in hepatic abscess, 405, 407 

in Hodgkin's disease, 407 

in hysteria, 415 



INDEX 



S A i> 



Fever in infantile spinal paralysis, 95, 

99 

in infectious diseases, 394 

in influenza, 412 

in injuries to spinal cord, 415 

in intermittent malarial fever, 403 

in Malta fever, 400 

in measles, 402 

in mild gastro-intestinal catarrh in 

children, 394 
in miliary tuberculosis, 412 
in multiple neuritis, 414 
in pemphigus, 159 
in pernicious anemia, 407 
in pulmonary tuberculosis, 411 
in pyelitis, 355, 407 

suppurative, 407 
in relapsing fever, 401 
in remittent malarial fever, 407 
in rotheln, 402 
in scarlet fever, 401 
in septic poisoning, 405 
in septicemia, 407, 411 
in smallpox, 403 

secondary, 155 
in syphilis, 414 
in teething, 394 
in thermic fever, 414 
in tonsillitis, 204 
in trichinosis, 400 
in typhoid fever, 394 
in typhus fever, 400 
in ulcerative endocarditis, 399, 405 
in Weil's disease, 408 
in yellow fever, 408 
infantile remittent, 408 
nails in, 50 
rapid pulse in, 280 

respiration in, 216 
relapsing, 401 
remittent, 407 

septic, in purulent cystitis, 343 
sighing or arhythmic respiration in, 

in children, 24 
significance of, 393 
thermic, 414 

urethral, from passing sounds, 394 
urine decreased in, 348 
Fibrinous bronchitis, small casts of 

bronchial tubes in sputum in, 477 
Fibroid nodules, subcutaneous, in 

rheumatism, 141 
phthisis, inspection of chest in, 246 
Filaria, embryos of, in urine, 352 
hematuria in, 351 
sanguinis hominis, hematuria due 

to, 352 
Fingers, appearance of, diagnostic of 

chloral habit, 50 
clubbed, in heart disease, 49 
fixation of joints of, 51 
in gout and arthritis deformans, 51 
in syphilitic dactylitis, 50 



Fingers, spasm of, due to occupation, 

61 
"Fish-mouth" of nasal obstruction, 

2 9 

Fissure of the anus, diarrhea in, 

333 

pain in, 492 
Flat-foot in locomotor ataxia, 102 
Flint's murmur, 266 
Floating kidney, 323 
pain in, 489 
liver, 320 
spleen, 327 
Fluoroscope in diagnosis of aortic aneu- 
rysm, 272 
of tuberculosis, 248 
Follicular enterocolitis, mild, 334 

tonsillitis, symptoms of, 204 
Fontanelle, condition of, diagnostic, 

46 
Foot-and-mouth disease in man, erup- 
tion in, 199 
Foot-drop, 99 

Forehead, immense and bulging, with a 
wizened, puny face beneath, indi- 
cating hydrocephalic tendencies, 
28 
square and projecting, in rickets, 

28 
wrinkled, indicating pain in head, 

2 7 
Foreign body in air passages, 256 

in bowel, 316 
Formication, 76, 170 
Fovea centralis, 386 
Fremitus, vocal, decrease of, 221 

increase of, 221 

mode of production of, 220 
Friction sounds, 239 

at apex of chest, due to tubercu- 
losis, 239 

due to pleuritis, 239 

heard in axilla, 239 

pericardial, 239, 269 
Friedreich's ataxia, claw-foot in, 101 

diagnosis of, 496 

differential, between locomotor 
ataxia and, 78 

diplopia a symptom of, 361 

face of, 31 

gait of, 73, 78 

knee-jerk in, 495 

movement of hands in, 66 

nystagmus in, 373 

sensory disturbance of skin in, 
176 

slow, scanning speech in, 127 
Frog-belly, 300 
Frost-bite, gangrene in, 54 
Fungus foot disease. 108. See Myce- 
toma. 
Furunculosis, 158 

in diabetes mellitus, 3 v s8 



5i6 



INDEX 



Gait, 73 

"astasia abasia, 82 

in acute poliomyelitis, 80 

in cerebellar disease, 81 

tumor, 82 
in chronic myelitis, 79 
in disseminated sclerosis, 78 
in Friedreich's ataxia, 78 
in general paresis, jy 
in gout, 73 
in health, 18 
in hemiplegia, 82 
in hereditary cerebellar ataxia, 78 
in Huntingdon's chorea, 452 
in hysteria, 82 

in infantile cerebral paralysis, 81 
in lateral sclerosis, 80 
in locomotor ataxia, 73, 78 
in multiple sclerosis, 79 
in neurasthenia, 18 
in osteomalacia, 83 
in paralysis agitans, 81 
in pseudomuscular hypertrophy, 80 

-tabes, 75 
in rheumatism, 73 
in rickets, 80, 81, 83 
in sciatica, 73 
Gall-bladder, cancer of, 321 
diagnosis of obstruction of, 321 
enlargement of, causes of, 321 
hydrops of, 321 
Gall-stone colic, 321, 485 

in catarrhal or suppurative cho- 
langitis, 405 

in stools, 338 

jaundice in cases of, 133 
stones, enlargement of gall-bladder 

due to. 321 
Gangrene in central nervous lesion, 159 
diabetic, of toes, 106 
in diabetes, 106, 160 
in embolism, 107 
in ergotism, 54, 159 
in exophthalmic goitre, 107 
in frost-bite, 54 
in leprosy, 54 
in nerve injury, 159 
in Raynaud's disease, 54, 160 
of extremities, following infectious 
fevers, 107 

in diabetes mellitus, 160 
qf intestines, odor of stools in, 337 
of skin, 160 
pulmonary, due to putrid bronchitis, 

254 

fetid breath in, 19, 249 

mucopurulent stools in, 336 

sputum in, 249, 475, 476 

vomiting in, 469 
senile, perforating ulcer of foot in, 106 
spontaneous, in hysteria, 159 



Gastralgia, diagnosis of, 491, 492 
neuralgic spots in, 491, 492 
pain in, 491 
position in, 20 
Gastric cancer, fever in, 407 
indicanuria in, 355 
most frequent at pylorus, 312 
vomiting in, 312, 466 
catarrh, acute, tongue in, 194 
vomiting in, 456 
chronic, vomiting in, 456 
crisis in locomotor ataxia, 74 
dilatation, 304. See Dilatation of 

stomach, 
disorders, odor of breath in, 19 
ulcer, anemia in, 313 
pain in, 313, 483 
vomiting of blood in, 466 
Gastritis, vomiting in, 456 
Gastroduodenal catarrh, jaundice in, 

133 

Gastroptosis, Glenard's belt sign of, 307 
jaundice as result of, 135 
x-rays in diagnosis of, 306 
General anasarca in acute diffuse 
nephritis, 356 
in advanced cancerous cachexia, 

164 
in arsenic poisoning, 164 
in beriberi, 163 
in children with acute diffuse 

nephritis, 357 
in chronic parenchymatous ne- 
phritis, 357 
diagnostic considerations, 17 
in heart disease, 163 
in multiple peripheral neuritis, 163 
in renal disease, 163 
Geographical tongue, 199 
Gerhardt's symptom of thrombosis of 

lateral sinus, 429 
German measles. See Rotheln. 
Girdle sensation, 188 

in locomotor ataxia, 188 
in transverse myelitis, 87, 88, 188 
in tumors of cord and meninges, 
188 
Glanders, eruption of, 145 
Glaucoma, dilated pupil in, 360 

headache in, 419 
Glenard's belt sign of gastroptosis, 307 
Globus hystericus in hysteria, 447 
Glossitis, acute, 199 
chronic superficial, 198 
dissecting, 196 
Glossodynia exfoliativa, 198 
Glossolabiopharyngeal paralysis, 41 
cardiac feebleness in, 277 
cough in, 473 
dysphagia in, 206 
tongue in, 200, 202 

bilateral atrophy of,_ 199 
Gmelin's test for bile in urine, 354 






INDEX 



517 



Goitre, exophthalmic, Abadie's sign in, 

43. 48 
brown pigmentation in, 139 
exophthalmos in, 48, 359 
gangrene in, 106 
Graefe's symptom of, 359 
leukoderma in, 139 
localized sweating in, 162 
Moebius' sign of, 360 

paroxysmal bloody, mucous diar- 
rhea in, 336 
Stellwag's symptom in, 360 
symptoms of, 359 
tache cerebrale in, 144 
tachycardia in, 48, 276 
thrill over carotid arteries in, 276 
tremor of hand in, 65 
vomiting in, 458 
Gonococci a cause of empyema, 252 
Gonorrheal arthritis, acute, 102 
Gout, aortitis in, 482 
fingers in, 51 

hyperesthesia of scalp in, 189 
joint affections in, 105 
limping gait of, 73 
nails in, 51 

pain in great toe in, 492 
plumbic, 105 
pruritus in, 190 
retinal hemorrhages in, 389 
Gouty diathesis, nails in, 50 
Graefe's spots, 43 

symptom, 359 
Graves' disease, tremor of hand in, 65 
"Grisolle" sign of smallpox, 146 
Grocco's sign in pleural effusion, 251 
Groins, 328 
Gumma, syphilitic, 422 

of liver, 303 
Gums, blue line on, in lead poisoning, 

20 3 

spongy, in salivation, 203 
in scurvy, 203 



Habit chorea, 62 

spasm, 42, 62 
Hands, "accoucheur's," in tetany, 60 
and arms, 49 

general movements of, 65 
physical examination of, 72 
tremors of, 63 
changes in shape of, in amyotrophic 
lateral sclerosis, 58 
in chronic rheumatism, 52 
choreic movements of, in children 

with chorea minor, 61 
claw-, 55 

in Morvan's disease, 58 
cold and clammy, due to bromidro- 
sis, 51 



Hands, cold and clammy, due to local 
innervation of sweat glands, 51 
contractions of, following apoplexy, 

59 
from hysteria, 60 

distribution of anesthesia of, in neu- 
ritis, 181, 182, 183 

Dupuytren's contraction of, 52 

flexion of, in cerebral palsy of chil- 
dren, 59 

gangrene of, 54 

in acute articular rheumatism, 53 

in angioneurotic edema, 54 

in child with cerebral trouble, 24 
with heart disease, 49 

in emphysema and chronic phthisis, 

49 
in heart disease, 20 
in meningeal congestion or hydro- 
cephalus in children, 60 
in thoracic aneurysm, 49 
inspection of, 49 
lateral drop of, in neuritis or acute 

infantile poliomyelitis, 61 
seal-fin, in arthritis deformans and 

gout, 52 
spade-like, 55 
spasm of, 62 
sweating of, in progressive muscular 

atrophy, 51 
'swelling and rupture of, 55 
tremors of, 63 
wasting of , 55 

with flexion and rigidity rarely 
seen in paralysis agitans, 59 
Harrison's grooves in rickets, 213 
Haut mal, 491 
Hay fever, 412 
Haygarth's nodosities, 52 
Head, examination of, 44 
excessive sweating of, 47 
in acromegaly, 46 
in advanced strabismus, 45, 365 
in chorea infantum, 331 
in chorea minor, 44 
in chronic deafness, 45 
in cretinism, 46 
in hydrocephalus, 46 
in idiocy, 46 
in mental depression, 46 
in microcephalus, 46 
in myxedema, 46 
in osteitis deformans, 46 
in peritonitis, 20 
in rickets, 46, 48 
neuralgia of, 479 
retraction of, 45 

tremor in disseminated sclerosis, 64 
Headache, causes of, 416 
due to chloral habit, 419 

to hemorrhage, 431 
from use of drugs, 419 
in anemia, 431 



5*8 



INDEX 



Headache in anterior poliomyelitis, 95 
in auto-intoxication, 418 
in brain abscess, 414 

tumor, 420, 459 
in cerebral tumors, 459 
in cerebrospinal meningitis, 410 
in croupous pneumonia, 430 
in dental caries, 431 
in diabetes, 420 
in digestive disturbances, 416 
in disease of cranial bones, 431 
in ear disease, 431 
in exposure to cold, 431 
in eye-strain, 418 
in glaucoma, 419 
in hematoma of the dura, 430 
in hemi crania, 417 
in intermittent fever, 431 
in intracranial aneurysm, 431 
in iritis, 419 
in jaundice, 417 
in malaria, 431 
in Malta fever, 400 
in measles, 430 
in meningeal hemorrhage, 430 

tumors, 420 
in meningitis, 420, 460 
in migraine, 417 
in nasal catarrh, 431 
in nervous exhaustion, 419 
in neurasthenia, 419 
in nocturnal epilepsy, 431 
in phosphaturia, 419 
in phosphorus poisoning, 468 
in renal disease, 419 
in rheumatism, 419 
in smallpox, early stages, 430 
in sunstroke, 430 
in syphilitic arteritis, 422, 423 

epilepsy, 443 

gumma, 422, 423 

meningitis, 422, 423 
in tuberculous meningitis, 425 
in typhoid fever, 430 
in typhus fever, 400 
in uremia, 419, 420 
in valvular heart disease, 431 
vomiting in, 456 
Heart, alterations in area of dulness of, 

229 
apex beat of, 221, 222 

displacement of, to left, 222 
to right, 222 

raised, 222 

strength of, 222 
arrhythmia of, 275 
asthma due to lesions of, 255 
block, 264, 275, 276 
blood-streaked sputum in valvular 

lesions of, 475 
causes of pain in neighborhood of, 

481 
congenital disease of, 268 



Heart, cough in valvular disease of, 472 
dilatation of, 223, 231, 273 

in acute diffuse nephritis, 356 
disease of, appearance of hands in 
children in, 49 

cyanosis in, 140 

edema in, 163 

hematemesis in, 467 

jaundice in chronic valvular, 135 

patient's position in, 20, 21 

retinitis, in 388 
extra systoles of, 281 
failure, in influenza, 274, 412 

unconsciousness in, 433 
fatty degeneration of, 276 

deposition on, 276 
general malformation of, 268 
headache in valvular disease of, 431 
hypertrophy of, 275 

in chronic parenchymatous neph- 
ritis, 357 
in chronic interstitial nephritis, 357 
location of murmurs of, 260, 261 
murmurs, significance of, 260, 261 
neuroses of, 275, 276 
percussion of, 228 
rapid, 276 

in exophthalmic goitre, 276 
secondary diphtheritic dysentery in 

chronic disease of, 335 
sounds, 258 

accentuation of, 259 

normal, 258 

reduplication of, 260 

where best heard, 260 
symptoms associated with murmurs 

of, 268 
thrills of, 223 
tobacco, 275 

valvular lesions of, 262-269 
Heat exhaustion, subnormal tempera- 
ture in, 415 
stroke. See Sunstroke, 
prostration, diarrhea due to, 332 
Heberden's nodes, 52 
Heel and toe, tender, in sciatica, 484 
Hematemesis, as vicarious menstrua- 
tion, 467 
diagnosis between hemoptysis and, 

467 

due to swallowed blood, 467 

in acute yellow atrophy of liver, 467 

in cirrhosis of liver, 467 

in dengue, 467 

in gastric cancer, 466 

ulcer, 466 
in heart disease, 467 
in hemophilia, 467 
in influenza, 467 
in injury of stomach, 467 
in locomotor ataxia, 467 
in malaria, 467 
in melena neonatorum, 467 



INDEX 



5 J 9 



Hematemesis in purpura hemorrhagica, 

467 
in relapsing fever, 467 
in scurvy, 467 
in typhus fever, 467 
in yellow fever, 467 
Hematogenous jaundice, 136 
Hematoma auris, 143 

of dura, headache in, 430 
subperiosteal, in children, 105 
Hematuria, acute, 349 

blood from bladder in, 349 
from kidney in, 349 
from urethra in, 349 
chronic, 350 
Hemiachromatopsia, 382 
Hemianesthesia due to lesion of optic 
thalamus, 172 
in apoplexy, 172 
in capsular disease, 171 
in chorea, 173 
in cortical lesions, 171 
in disseminated sclerosis, 172 
in hysteria, 170, 382 
in softening of brain, 172 
in tumor of brain, 173 
partial, with partial hemiplegia on 
opposite side, due to lesions of one 
side of cord, 173 
Hemianopsia, 376, 378 
binasal, 379 
bitemporal, 379, 381 
homonymous, 379, 380 
in brain tumor, 421 
in hysteria, rarely, 170, 383 
in migraine, 456 
location of lesion in, 379 
method of determining, 379 
use of perimeter in determining, 380 
Hemiatrophy, facial, 32 

of tongue, 200 
Hemicrania. See Migraine. 
Hemidyschromatopsia, 382 
homonymous, 382 
in hysteria, 383 
Hemihypertrophy, facial, 33 
Hemilateral myelitis, symptoms of, 99 
Hemiopic pupillary inaction, 376, 422 
Hemiplegia, bed-sores in, 160 
brain areas involved in, 112 
crossed, due to bulbar lesions, 123 
diagnosis of, 118 

from acute infantile paralysis, 122 
from cerebellar hemorrhage, 121 
from cerebral hemorrhage, 117 
in crus cerebri, 124 
in frontal lobe, 1 19 
in internal capsule, 118 
in island of Reil, 121 
in occipital lobe, 119 
in parietal lobe, 118 
in pons Varolii, 123 
location of lesion in, 118 



Hemiplegia from diffuse cerebral sclero- 
sis of one hemisphere, 122 

from disseminated sclerosis, 122 

from hematoma of dura mater, 122 

from syphilis, 122 

gait in, 82 

hyperesthesia in, 189 

in cerebral embolism, 121, 122 
thrombosis, 121 

in ingravescent apoplexy, 119 

in locomotor ataxia, 122 

in paretic dementia, 123 

in purulent meningitis, 123 

in renal disease with uremia, 123 

irregular forms of, 121 

nails in, 50 

pupillary immobility in, 375 

spastic, 122 
infantile, 59 

symptoms associated with, 117, 118, 
119 

tongue in, 195 
Hemoglobinuria, paroxysmal, 352 

signs of, 352 

urine in, 469 

vomiting in, 469 
Hemometer. See Hemoglobinometer. 
Hemophilia, 352 

hematemesis in, 467 

hematuria in, 352 

hemoptysis in, 475 

hemorrhage into retina in, 389 

joint involvements in, 106 
Hemoptysis, currant-jelly clots in, 475 

diagnosis of, 467, 475 
Hemorrhage, cerebellar, 121 

cerebral, causing hemiplegia, 117 
diplopia a symptom of, 361 
hiccough in, 455 
ocular paralysis, 366 
vomiting in, 459 

facies in, 3 1 

from mucous membrane in yellow 
fever, 408 

from stomach, 467 

in Banti's disease, 326 

in typhoid fever, 395 

indicated by anxious restlessness, 20 

into lesser peritoneum, 316 

into membranes of cord, 96 

into retina, 388, 389 

into skin, 143 

into spinal cord, 106 

into paraplegia in, 106 

jaundice after severe prolonged, 136 

meningeal, symptoms of, 120, 430 

pallor of face in, 26 

pulmonary diseases in which it 
occurs, 474, 475 

subdural, cause of, 438 

ventricular, differential diagnosis 
between meningeal hemorrhage, 
120 



520 



INDEX 



Hemorrhagic infarction of intestine, 
3i6, 464 

pancreatitis, acute, 316 

pleural effusion, 253 

pleurisy, 253 

retinitis, 388 
Hemorrhoids, blood in stools caused by, 

337 
pruritus due to, 190 
Henoch's disease, 143 
Hepatic abscess, fever in, 405 
tongue in, 195 
cirrhosis, enlargement of spleen in, 
326 
hematemesis in, 467, 469 
jaundice in, 135 
with pigmentation, 136 
colic, 133, 485 

retraction of abdominal wall in, 

300 

disease, constipation in, 329 
Hepatitis. See Abscess, hepatic. 
Hepatogenous jaundice, 132, 133 
Hereditary spastic paraplegia, 86 
Hernia, umbilical, 326 
Herpes labialis after salicylic acid, 158 
in croupous pneumonia, 29, 158 
in epidemic spinal meningitis, 
158 
zoster, 158 
Hiccough, 455 ^ 
Hip disease, pain in, 22, 483, 484 

spontaneous dislocation of, following 
infectious disease, 106 
Hippocratic face, 31, 331 

succussion, 242 
Hippus, 376 
His' bundle, 275, 279 
Hodgkin's disease, enlargement of 
cervical lymphatic glands in, 
48,407 
temperature in, 407 
Hollow chest an indication of tubercu- 
losis, 18 
Horse-shoe kidney, 316 
Hour-glass stomach, 307 
Huntingdon's chorea, 63, 452 
Hutchinson pupil in cerebral hemor- 
rhage, 120 
teeth, 203 
Hydatid cyst of liver, 320 

disease of spleen, 327 
Hydrarthrosis, chronic, 103 
Hydrocephaloid disease, 450 

state, 47 
Hydrocephalus, contraction of hands 
and arms in, 60 
face in, 28 
head in, 46 
nystagmus in, 373 
open fontanelle in, 46 
spastic rigidity of arms in, 60 
Hydronephrosis, 324 



Hydropneumothorax, coin percussion, 
252 
Hippocratic succussion in, 242 
metallic tinkling in, 239 
physical signs of, 252 
Hydrops of gall-bladder, 321 
Hyperesthesia, 188 

following the use of drugs, 190 

in anemia, 190 

in brain tumor, 189 

in cerebrospinal meningitis, 189 

in chronic alcoholism, 189 

leptomeningitis, 189 
in gout, 189 
in hemiplegia, 189 
in hysteria, 170, 188 
in influenza, 190 
in leprosy, 190 
in locomotor ataxia, 189 
in menopause, 189 
in myelitis, 189 
in neuralgia, 189 
in neurasthenia, 188 
in peripheral neuritis, 189 
in poisoning by lead and arsenic, 189 
in relapsing fever, 190 
in rickets, 189 
in scurvy, 189 
in transverse, myelitis, 189 
in typhoid fever at convalescence, 
189 
Hyperpyrexia. 390 

Hypertrophy, cardiac, apex beat in, 
221 
in aortic regurgitation, 267 
associated with chronic contracted 
kidney, increase of urine in, 348 
diagnosis of, 275 

in chronic interstitial nephritis, 

. 357 
limited bulging of chest in, 213 

of nails in, 5c 
pulse in, 280 

pseudomuscular, gait in, 80 
symptoms and signs of, 275 
Hypochondrium, tenderness of, 319 
Hypotonus in locomotor ataxia, 74 
Hysteria, allochiria in, 187 

alterations of color fields in, 382 

anesthesia in, 170 

aphonia in, 125 

bilateral anesthesia in, 173 

brachial monoplegia in, 68 

bromidrosis in, 162 

contractions of hands, feet, and legs 

in, 60 
convulsions in, 445 
diagnosis of, 445-447, 450 
diarrhea in, 336 
dilated pupil in, 360 
emprosthotonos in, 446 
facial paralysis in, 36 
spasm in, 44, 447 



INDEX 



52i 



Hysteria, false clonus in, 497 

fatuous expression in, 30 

fever in, 415 

gait in paralysis of, 82 

gauntlet or stocking form of anes- 
thesia in, 173 

globus hystericus in, 447 

hemianesthesia in, 170, 382 

hemianopsia rare in, 170, 381, 382 

hemidyschromatopsia in, 382 

hemorrhages into skin in, 143 

hiccough in, 455 

hippus rare in, 376 

hysterogenous zones of hyperesthesia, 
in, 188 
localized sweating in, 162 

mirror writing rare in, 66 

nodding spasm in, 44 

ocular symptoms of, 383 

opisthotonos in, 446 

pain, cutaneous, in, 190 

painful joints in, 484 

paraplegia in, 83, 97 

phantom tumor in, 325 

ptosis in, 40 

respirations in, 217 

spasm of esophagus in, 207 
of tongue in, 202 

spontaneous gangrene of skin in, 159 

squint in, 372 

status epilepticus in, 446 
• subnormal temperature in, 415 

tremor of hands in, 65 

urine increased in, 347 

visual changes in, 171 

vomiting in, 457 

wry-neck in, 44 
Hysterical chorea, 62 

mutism, 125 

paralysis, 82 
Hystero-epilepsy, diagnosis of, 447 
Hysterogenous zones, 188 



"Iced" liver, 320 
Ichthyosis of tongue, 198 
Icterus. See Jaundice, 
neonatorum, 137 
urobilin, 136 
Idiocy, 46 

amaurotic family, 84 
Idiopathic epilepsy, 443 
Idiosyncrasy to drugs, 18, 143 

hemoglobinuria of, 352 
Impaction of feces, 316 
Impetigo contagiosa, eruption in, 157 
Incontinence of urine, 18 

due to concentrated urine, 345 
to excessive reflex irritation of 

bladder walls, 345 
to insensitive urethra, 345 



Incontinence of urine, due to loss of 
power of sphincter, 345 
erythema of thighs in, 150 
nocturnal, in children, 345 
trousers stained in, 18 

Incubation period of eruptive diseases, 

154 

Indicanuria, 355 

diseases in which it occurs, 355 
test for, 355 
Indigestion, acute, roseola of, 147 
headache associated with, 416 
hiccough in, 455 
intestinal pain in, 483, 485 
muscae volitantes in, 383 
respiration of child with, 24 
retraction of head in neurotic chil- 
dren with, 45 
vertigo in, 432 
Infantile cerebral paralysis, gait in, 
81 
movements of hand in, 66 
hemiplegia, spastic, 59, 122 
remittent fever, 408 
spinal paralysis. See Anterior polio- 
myelitis. 
Infarction, hemorrhagic, of intestine, 
316, 464 
pulmonary hemoptysis in, 474 
hematuria in, 350 
Influenza, epidemic, cardiac failure in, 
412 
catarrhal symptoms of, 412 
complications of, 412 
diarrhea, 412 
differential diagnosis from dengue, 

408, 409 
fever in, 412 
hematemesis in, 467 
hyperesthesia in, 190 
microorganism of, as cause of, 

empyema, 252 
ocular palsy in, 368 
sputum in, 474, 475 
vomiting in, 412 
Ingravescent apoplexy, 119 
Insomnia in Malta fever, 400 
Inspection of chest, 208 

of abdomen, 299 
Interlobular pleurisy, physical signs of 

252 
Intestinal crises in locomotor ataxia, 
332 
hemorrhage in typhoid fever, 395 
indigestion, pain in, 487 
obstructidn, 316 

albumin in urine, 463 
constipation in, 330 
due to cancer or stricture , 464 
to impaction of foreign body, 

464 
to intussusception, 461 
to strangulation by bands, 462 



22 



INDEX 



Intestinal obstruction, due to strangula- 
tion, diverticulum, 463 
to volvulus, 464 
hiccough in, 455 
indicanuria in, 355 
vomiting in, 460 
parasites, 338 
perforation, pain in, 489 
rigidity, 325 

vomit in, 470 
sand, 338 
Intestine, hemorrhagic infarction of, 

464 
Intra-ocular muscles, paralysis of, 373 
Intussusception, sloughing of bowel in, 
338 
pain in, 460, 461 
vomiting in, 460 
Iodophilia, vomiting in, 460 
Iritis, headache due to, 418 

immobile pupil in, 360 
Irregular breathing, 236 
Irritative mydriasis, 375 

myosis, 375 
Itching of jaundice, 190 



Jacksonian epilepsy, 441, 442 
Jacquet's sphygmocardiograph, 284 
Jaundice, 132 

as result of gastroptosis, 135 

bradycardia in, 276 

catarrhal, 133 

Charcot's fever in, 134 

constipation in, 329 

diabete bronze in, 136 

fatty diarrhea in, 336 

from cerebral concussion, 137 

from fright or extreme anger, 137 

hematogenous, 136 

headache in, 417 

hepatogenous, 132 

in acute phosphorus poisoning, 135 
ulcerative endocarditis, 137 
yellow atrophy, 136 

in amyloid liver, 135 

in cholangitis, 407 

in chronic valvular heart disease, 135 

in cirrhosis of liver, 135 

in croupous pneumonia, 137 

in diabetes, 135 

in disease of pancreas, _ 135 

in echinococcus of liver, 135 

in malignant disease, 134 

in newborn, 137 

in pressure from aneurysm, 133 

in remittent malarial fever, 407 

in Weil's disease, 135, 408 

in yellow fever, 135, 408 

itching of, 190 

obstructive, 133 



Jaundice, persistent and progressive in 
carcinoma of pancreas, 315 

pruritus in, 190 

purpuric eruption in severe, 143 

pyemic, 137 

stools in, 133, 136, 337 

sweating in, 162 

tongue in, 193 

urine in, 136, 353, 354 

vomiting in, 458, 469 
Joints, 102 

alterations of, 103 

hypertrophic osteoarthritis following 
typhoid fever, 104 

in acute epiphysitis of infancy, 

I0 5 

synovitis, 103 
in central myelitis, 102 
in cerebrospinal meningitis, 102 
in chronic lead poisoning, 105 
in dengue, 105 
in gonorrheal arthritis, 102 
in gout, 105 
in hemophilia, 106 
in milk leg, 106 
in osteomyelitis, 104 
in rheumatoid arthritis, 103 
in scarlet fever, 106 
in Schonlein's disease, 105 
involvement of, with fever, 414 
pain on motion of, in Malta fever, 

400 
small, in Morvan's disease, 102 

in syringomyelia, 102 
Jumpers, the, 63, 453. See Saltatoric 
spasm. 



Kernig's sign in meningitis, 427 
Kidney, blood in urine from, 338, 349, 

351 
cancer of, hematuria due to, 351 
chronic contracted, reduplication of 

heart sounds in, 260 
cystic degeneration of, 303, 324 
floating, 323, 489 
hematuria due to stone in, 351 
horse-shoe, 316 
hydronephrosis, 324 
pain in, 489 

hematuria due to, 349 
tuberculosis of, 351, 490 
Klumpke's paralysis, 70 
Knee-jerk, diseases in which it is 
decreased, 495 
in which it is increased, 496 
how best elicited, 494 
in locomotor ataxia, 74 
reinforced, 494 
testing of, 108 
Kyphosis, 33 



INDEX 



523 



La grippe. See Influenza. 
Landouzy-Dejerine type of muscular 

atrophy, 31 
Landry's paralysis, diagnosis of, 96, 

415 

from acute central myelitis, 96 
loss of knee-jerk in, 495 

of reflexes, predominant symp- 
tom of, 415 
non-spastic paraplegia in, 96 
Laryngeal crises in locomotor ataxia, 

74 

obstruction, cyanosis due to, 140 

paralysis, 126 

phthisis, cough in, 473 

spasm, 256 
Laryngismus stridulus in tetany, 451 
Laryngitis, night cough in, 473 

partial or complete loss of voice in, 

473 
short, sharp, brassy cough in, 473 
whispering voice in, 125 
Lead colic, retraction of abdominal 
wall in, 300 
epilepsy, 444 

chronic paralysis in, 61 
gait in, 75 

peripheral neuritis in, 181 
poisoning, blue line on gums in, 203 
tremors in, 63 
Leg, milk, 106 

paralysis of, 100 
Legs, feet and, 73 

deformities of, 101 
swelling of, 106 
Leprosy, appearance of hands in, 54 
gangrene in, 54 
hyperesthesia in, 190 
leonine face of, 32 
Leptomeningitis, diagnosis of coma in 
purulent, 438 
hyperesthesia in chronic, 189 
Leukemia, hematuria in, 352 

splenomedullary, enlargement of 
spleen in, 326 
Leukocythemia. See Leukemia. 
Leukocytosis, in cholangitis, 457 
Leukoderma in goitre, 139 
Leukokeratosis buccalis, 198 
Leukoma of tongue, 198 
Lichen planus, tongue in, 199 

ruber, nails in, 50 
Lienteric diarrhea, 333 
Light, pupillary, reaction to, 374 
Lingual paralysis, 200 

ulcers, 197 
Lips, fulness of, in persons of strong 
sexual appetite, 26 
indicating phlegmatic tempera- 
ment, 26 
greatly thickened in cretinism, 31 



Lips, immobility of, due to mucous 
patches or ulceration of buccal 
mucous membrane, 29 

pendulous, in progressive bulbar par- 
alysis, 41 

slightly parted, dry, and cyanotic in 
chronic pulmonary or cardiac dis- 
ease, 29 

thin and mobile, in nervous indi- 
viduals, 26 

twitching of raised upper, in peri- 
tonitis or pain below diaphragm, 29 
Litten's sign, 219 

Liver, acute yellow atrophy of. See 
Yellow atrophy, acute. 

amyloid disease of, jaundice in, 135 

causes of tenderness of, 319, 320 

cirrhosis of, hematemesis in, 467 
bulging of abdominal wall in, 303 
jaundice in, 135 

enlargement of, 303 
position in, 20 

floating, 320 

hematemesis in, 467 

headache in congestion of, 418 

hydatid cyst of, 320 

indicanuria in cancer of, 355 

jaundice in, 135 

malignant disease of, jaundice in, 

134 
nodules and umbilication of, in, 

3i8 .. 
in syphilis, 318 
percussion note over, 225, 317 
pushed down by right-sided pleural 

effusion, 318, 320 
rough, in cirrhosis, 318 
swelling of, in Weil's disease, 408 
symptoms of cirrhosis of, 318 
of malignant disease of, 318 
of tropical abscess of, 320 
vomiting in, 469 
Localization of functions of segments of 

spinal cord, 90, 93 
Localized sweating, 162 
Locomotor ataxia, 73 
allochiria in, 187 
analgesia in, 174 
anesthesia of lower portion of body 

and of legs in, 174 
Argyll-Robertson pupil in, 74, 374 
athetoid movements in, 66 
bladder symptoms of, 344, 351 
blunted and delaved sensation in, 

174. 
brachial monoplegia in, 69 
cardiac feebleness in, 277 
coffee-ground vomit in gastric 

crisis of, 457 
contracted pupil in, 375 
cutaneous hemorrhages in. 143 
diagnosis o\, 405 

from Friedreich's ataxia, 78 



5 2 4 



INDEX 



Locomotor ataxia, diagnosis of, from 
general paresis, 174 
from hereditary cerebellar ataxia, 

from hysteria, 76, yy 
diarrhea as an intestinal crisis of, 

332 
dilatation of pupil in, 376 
diplopia in, 361 
double sciatic pain in, 481, 483, 

490 
flat-foot in, 102 
gait of, 73 _ 

gastric crisis of, 74, 467 
girdle sensation in, 188 
hematuria in, 351 
hemiplegia in, 122 
hyperesthesia in, 189 
hypotonus in, 74 
inability to use fingers and hands 

in, 66 
joints in, 103 
intestinal crisis in, 332 
laryngeal crisis of, 74 

spasm in, 256 
lesion of optic nerve in, 388 
loss of knee-jerk in, 74, 495 
muscular atrophy of arm in, 69 

hypotonus in, 74 
numbness of feet in, 74 
nystagmus in advanced, 373 
ocular symptoms of, 388 
optic atrophy in, 388 
pain in, 481, 484, 491 

of skin in, 190 
paraplegia in, 88, 95 
paresthesia in, 187 
perforating ulcer in, 106 
ptosis in, 40 ,361 
retention of urine in, 344 
Romberg's symptom of, 74 
swaying of body in, 74, 1 1 1 
syphilis a frequent cause of, 73 
thoracic pain in, 482 
tongue in, 199 
twitching of fingers in, 66 
vesical crisis of, 74, 351 
Westphal's sign of, 74 
Lordosis in cretinism, 32 

in progressive muscular atrophy, 57 
Ludwig's angina, 205 
Lumbago, pain in, 483 
Lumbar puncture, 410 

in diagnosis of cerebrospinal men- 
ingitis, 410 

of tuberculous meningitis, 426 
Lupus, ulceration of tongue in, 197 
Lymphangioma, congenital, tongue in, 

199 
Lysis, fever in erysipelas, ending by 

crisis or, 403 
in scarlet fever, ending by, 401 
in smallpox, ending by, 403 



Lysis, fever in typhoid, ending by, 395 
in catarrhal pneumonia, 413 
rare in croupous pneumonia, 413 



M 



McBurney's point, 488 
Macroglossia, 199 
Macula lutea, 386 
Maddox-rod test, 363 
Madura foot, 55, 108 
Main en griffe,55 
Malaria, aortitis rare in, 482 
brow ague in, 479 
Cheyne-Stokes breathing in hema- 

turic, 217 
chill in, 390 
coma in, 437 

enlargement of spleen in, 326 
headache in, 431 
hematemesis rare in, 467 
hematuria in, 349 
hemoglobinuria in, 352 
intermittent, attacks occurring ear- 
lier each day in, 405 
characteristic of fever, quartan, 
403, 404 
quotidian, 404 
tertian, 404 
chill, fever, and sweats in, 403 
diagnosis of, 404, 405 
effect of quinine on, 405 
pernicious, differential diagnosis be- 
tween yellow fever and, 409 
remittent, bilious vomiting in, 407 
character of fever in, 407 
diagnosis between typhoid fever 
and, 408 
between yellow fever and, 408 
due to estivo-autumnal parasite, 

407 
jaundice in, 407 
sweating in, 162 
synonyms of, 407 
retinal hemorrhage in, 389 
roseola in, 148 
splenic enlargement in, 326 
skin in, 138 
sweating in, 162 
Malignant pustule. See Anthrax, 

malignant. 
Malingering, convulsions in, 449 

inability to ape facies of disease in, 

26 
merycismus in, 470 
sciatica in, 485 
Malta fever, anorexia in, 400 
character of fever in, 400 
frequency of relapse in, 400 
headache in, 400 
insomnia in, 400 
pain on motion in, 400 



INDEX 



525 



Mammary gland, enlargement of, in 

pulmonary tuberculosis, 215 
Manchurian fever, 401 
Mania, acute, dilatation of pupil of, 376 
Maniacal chorea, 62 
Manometer, 288 
Marasmus, sinking in of fontanelle in, 

47 
Measles, character of fever in, 402 
date of eruption in, 154 
headache in, 430 
rash of, 153 

on pharynx and buccal mucous 

membrane, 128 
symptoms of, 153 
Meckel's diverticulum, 463 
Mediastinal abscess, diagnosis of, from 
mediastinal tumors, 258 
growths, cause of laryngeal spasm, 
256 
bulging of chest in, 213 
caput Medusas in, 303 
diagnosis of, from abscess, 257 
from aneurysm, 257 
from chronic pneumonia, 257 
from pericarditis, 257 
from pleural effusion, 257 
dysphagia in, 206 
hoarseness of voice due to pressure 

by, 125 
laryngeal cough due to pressure on 

larynx by, 473 
pain in, 482, 483 
signs and symptoms of, 257 
Mediastinopericarditis, indurative, pul- 
sus paradoxus in, 281 
epigastric pulsation in, 219 
hiccough in, 455 
Megrim. See Migraine. 
Melancholia, facial expression in, 30 

puerperal lingual spasm in, 202 
Melanotic cancer, black urine in, 348 
Melena neonatorum, vomiting in, 467 
Meniere's disease, symptoms of, 432 
vomiting following tinnitus au- 
rium and vertigo in, 456, 469 
Meningeal hemorrhage, 430 

irritation, tache cerebrale in, 144 
tuberculosis, Cheyne-Stokes respira- 
tion in, 217 
Meningitis, basilar, lesions causing ocu- 
lar paralysis in, 367 
papillitis in, 386 
retraction of head in, 45 
bilateral anesthesia in, 174 

loss of knee-jerk, 495 
bulging fontanelle in purulent, 47 
cerebrospinal. See Cerebrospinal 

meningitis, 
contracted pupil in, 360 
contraction of hand in, 60 
contralateral reflex in, 427 
delirium in, 427 



Meningitis, diplopia in, 361 
facial spasm in, 43 
hippus in acute, 376 
hyperesthesia in cerebrospinal, 189 
Kernig's sign, 427 
lumbar puncture, 410, 426 
nystagmus, 373 
occipital headache in, 460 
pain in nape of neck in, 460 
piercing cry in, 23 
pseudo-, 450 
purulent, hemiplegia in, 123 

vomiting in, 460 
reflexes in, 495 
retraction of head in, 45 
rigidity of dorsal muscles in, 460 
scaphoid belly in tuberculous, 300 
spinal, dilatation of pupil in, 375 

loss of knee-jerk in, 495 
subnormal temperature in, 415 
symptoms of, 422, 423, 424 
tache cerebrale in, 144 
tuberculous, 425 
papillitis in, 387 
reflexes in, 497 
vomiting in, 459, 460 
Menstruation, dark areas under eyes 
during, 26 
hematemesis as vicarious, 467 
hemoptysis as vicarious, 475 
Mercer sphygmomanometer, 296 
Mesentery, cysts of, 325 

tuberculosis of, 315 
Metallic tinkling heard over chest in 
cavity, 239 
over hydropneumothorax, 239, 

252 
over stomach, 239 
in pleural effusion with pneumo- 
thorax, 252 
Metatarsal neuralgia, 492 
Microcephalus, 46 
Microorganism of influenza, cause of 

empyema, 252 
Migraine, hemianopsia in, 456 
hyperesthesia in, 189 
muscae volitantes in, 383 
scotomata in, 456 
sweating of head in, 162 
symptoms of, 480 
vomiting in, 456 
Miliaria, 162 
Milk leg, joints in, 106 
Milky-looking urine, 355 
Mirror writing, 66 
Mitral disease, 262 
obstruction, 263 
regurgitation, 262 

accentuation of pulmonary second 

heart sound in, 262 
precordial thrill in, 263 
pulse in, 279 
symptoms of, 263 



526 



INDEX 



Mitral stenosis, 263 

auricular fibrillation in, 265 

heart block in, 265 

pulse in, 279 

reduplication of heart sounds in, 

260 
thrills in, 223 
Moebius' sign, 360 
Moist rales, 238 
Moller-Barlow's disease, 105 
Mono-anesthesia, 172 
Monoplegia, 66, 98 
brachial, 66 

bilateral, 70 
of lower extremities, 98 
Morbilli, 153. See Measles. 
Morphine as a cause of facial hemi- 
atrophy, 33 
Morton's painful toe, 492 
Morvan's disease, 58 

gangrene of hands in, 54 
small joints affected in, 102 
Mouth breathers, 29 
in heart disease, 29 
nasal twang of voice in, 126 
Mowing gait, 82 
Mucomembranous enteritis, 333 
Mucous disease, tongue in, 194 
membrane, buccal, 203 
patches about mouth and anus in 
infantile syphilis, 28 
immobility of lips due to, 29 
Multiple sclerosis. See Sclerosis, dis- 
seminated. 
Mumps, enlarged parotid glands in, 48 
Murmur, anemic, 261 
aortic aneurysm, 269 
regurgitant, 267 

capillary pulsation in, 267 

Corrigan's pulse in, 267 

dyspnea in, 267 

ox-heart in, 267 

pulsation of rentinal arteries in, 

267 
Quincke's sign of, 267 
short and sharp pulse in, 279 
water-hammer pulse in, 267 
stenosis, 266 

symptoms of, due to failing com- 
pensation, 267 
cardiopulmonary, 260 
heart, 260 

hemic, over fontanelle in rickets, 47 
mitral regurgitation,. 262 
murmur in, 262 
small volume of pulse in, 279 
symptoms of, due to failing 

compensation, 263 
thrill in, 263 
stenosis, 263 

auricular fibrillation in, 265 
heart block in, 265 
pulse wave of, 279 



Murmur, mitral stenosis, reduplication 
of second heart sound in, 260 
small volume of pulse in, 279 
symptoms of, due to failing com- 
pensation, 263 
thrill in, 263 
presystolic, 263 
pulmonary regurgitation, 268 
stenosis, 268 
valvular, 268 
tricuspid regurgitation, 268 
stenosis, 268 

systolic, in emphysema, 255 
Muscae volitantes, 383 
Muscle tone, 469 

Muscles, contraction of, in paramyo- 
clonus multiplex, 62 
in electric chorea of Bergeron, 62 
in Huntingdon's chorea, 63 
in "jumpers, 63 
intra-ocular, 373 

shock-like, in Dubini's disease, 62 
ocular, paralysis of, 361 
Muscular atrophy, faciohumeroscapular 
type of, 31 
hands in, 51 

idiopathic. See Atrophy, idio- 
pathic muscular, 
progressive, claw-hands in, 56 
diagnosis of, from Friedreich's 
ataxia, 101 
from multiple neuritis, 101 
from poliomyelitis, 101 
reflexes in, 497 
spastic monoplegia in, 100 
Mutism, hysterical, 125 
Myalgia, pain in, 483 
Mycetoma, 54, 108 
Mycoses, appearance of tongue due to 

growth of, 194 
Mydriasis, irritative, 375 
paralytic, 376 
unilateral, alternating, 376 
Myelitis, acute, ascending, 96 
central, 88 
disseminated, 79 
transverse, allochiria in, 187 
anesthesia in, 174 
bilateral in, 175 
bladder, symptoms of, 89, 343 
collateral symptoms, 344 
diagnosis of cervical, dorsal and 

lumbar, 90, 91, 92, 93 
effect of lesion in, 88 
girdle sensation in, 87, 188 
hyperesthesia in, 189 
knee-jerk in, 495, 496 
non-spastic, anesthesia in, 88 
bed-sores in, 88 
girdle sensation in, 96 
paraplegia in, 88 
reflexion in, 88 
paresthesia in, 187 



INDEX 



5 2 7 



Myelitis, acute, transverse, sensory 
paralysis in, 87 
spastic paraplegia in, 87 
symptoms of, 88 
chronic, gait of, 79 

transverse, differential diagnosis 
of lumbar, dorsal, and cervical, 
90 
hemilateral, 98, 99 
hiccough in, 455 
subacute, 89 
transverse, 88 

traumatic, retention of urine in, 343 
Myocarditis, degenerative, 277 
Myoclonus multiplex, 62 
Myosis in facial hemiatrophy, 32 
irritative, 375 
paralytic, 375 
Myotonia congenita, 63, 454 
Myxedema, enlargement of feet in, 101 
of tongue in, 200 
face of, 31 
head in, 45 
skin in, 140 
spade-like hand in, 55 



N 



Nails, atrophy of, 50 
hypertrophy of, 50 
in acute fevers, 50 
in anemia, 49 
in chloral habit, 50 
in eczema, 50 
in gout, 50 
in hemiplegia, 50 
in lichen ruber, 50 
in prolonged illness, 50 
in psoriasis, 50 

in pulmonary osteoarthropathy, 50 
in Raynaud's disease, 50 
in sclerodactyle, 50 
in syphilis, 50 
in syringomyelia, injury, or neuritis, 

50 
infantile palsy, 50 
white spots on, 50 
Nasal catarrh, chronic atrophic, breath 
in, 19 
headache in, 431 
obstruction, facial expression in, 29 
Nausea, acute, position in, 20 
Necator americana, 342 
Neck, spasm of muscles of, 44 
Necrosis fat, from impacted gall stone, 

321 
Nephritis. See also Kidneys and 
Bright's disease, 
acute, 356 
diffuse, 356 

hemorrhagic effusions in, 253 
irritation of bladder in, 345 



Nephritis, acute, parenchymatous, de- 
crease of urine in, 348 

chronic hemorrhagic, 349 
interstitial, 357 
high blood-pressure in, 290 
parenchymatous, 348, 357 
retinitis in, 388 
skin in, 140 
Nerve supply of iris, 373 
Nervous bladder, 346 

diarrhea, acute, 333 

exhaustion, headache in, 419 
Neuralgia, causes of, 479 

due to lead or arsenic poisoning, 479 

due to malaria, 479 

edema in, 165 

hyperesthesia in, 189 

intercostal, 482 

metatarsal, 492 

Morton's painful toe in, 492 

occipital, 481 

of fifth nerve, infra-orbital, 480 

of foot, 492 

of head, 479 

of labia majora or perineum, 483 

of pelvic viscera in women, 483 
pain in, 479 

sciatic, pain in, 484 

supra-orbital, diagnosis of, from neu- 
ritis, 479 
Neurasthenia, gait in, 18 

headache in, 419 

hyperesthesia in, 188 

increase in urine in, 347 

intestinal sand in, 338 

knee-jerk increased in, 498 

paresthesia in, 187 

scapulohumeral reflex in, 494 

vomiting in, 457 
Neuritis, acute multiple, fever in, 414 
knee-jerk lost in, 495 
symptoms and signs of, 414 

arsenical, gait in, 75 

cause of anesthesia, 180 

diagnosis of, 495 

diphtheritic, 181 

in foot, leg, and thigh, distribution 
of anesthesia in, 184 

in hand, distribution of anesthesia 
in, 181 

multiple, 414 

optic, 386. See Papillitis. 

peripheral anesthesia in, 181 
claw-hand in, 56 
general anasarca in, 163 
hyperesthesia in, 189 
nails in, 50 
skin in, 159 

retrobulbar, chronic, 387 

sciatic, diagnosis of, 484 
knee-jerk in, 41)5, 49(1 
limping gait of, 73 
pain in, 484 



528 



INDEX 



Neuritis, sciatic, tender joints in, 484 

toxic peripheral, 181 
Neuroma, pain in, 492 
Neurosis, cardiac, 275, 276 
Newborn, cyanosis in, 140 

jaundice in, 137 
Nicholson pocket sphygmomanometer, 
295, 296 

obstruction of bile ducts, 321 
Nictitating spasm, 43 
Night cough, 473 
Nodding spasm, 44 
Noma, 203 

Normal arterial tension, 287 
Nose, asthma due to reflex irritation in, 

2 55 

broad and flat, in cretinism, 31 
broadness of bridge of, an indication 

of congenital syphilis, 28 
dilated, in heart disease, 29 
in mouth breathers, 29 
pinched and drawn, indicating pain 

in chest in children, 27 
Nystagmus, 372 

in acute meningitis, 373 

in children, 373 

in disseminated sclerosis, 78, 372 

in epilepsy, 373 

in Friedreich's ataxia, 78, 373 

in growths in cerebellum or pons, 

373 

in hydrocephalus, 373 

in labyrinthine disease, 373 

in locomotor ataxia, advanced, 373 

in multiple sclerosis, 372 

in spastic paraplegia, 85 



Obermeier, spirillum of, 401 
Obstructive jaundice, 131 
Occupation spasm, 61 
Ochronosis, skin in, 138 

black urine in, 348 
Ocular muscles, paralysis of, 361 

paralyses, 361-373 
Oculofacial paralysis, 42 
Oculomotor paralysis, 361 
Omentum, tuberculosis of, 315 

tumors of, 315 
Onychogyrophosis, 50 
Ophthalmoplegia, 38 
Ophthalmoscopy, 384 
Opisthotonos in hysteria, 446 

in severe meningitis, 460 
Opium poisoning, 434 

differential diagnosis between poison- 
ing from alcohol and, 435 
Optic atrophy, 388 

nerve, 385 

neuritis, 386 
Orthophoria, 363 



Osteitis deformans, head in, 45 

of cranial bones, headache in, 431 
triangular face of, 33 
Osteomalacia, gait of, 82 
Osteomyelitis, acute, arthritis in, 104 
joint involvement with fever, 414 
Osteophytes, formation of, in rheuma- 
toid arthritis, 104 
Otitis in scarlet fever, 402 

media, with thrombosis of cavernous 
sinus, 429 
diagnosis between cerebrospinal 
meningitis and, 410 
vertigo in, 432 
Ovarian cysts, 300 

yellow color of skin in, 141 
"Ox-heart" of aortic regurgitation, 267 
Oxyuris vermicularis, 342 
Ozena, breath in, 19 



Pachymeningitis interna hemorrhag- 
ica, coma in, 438 
headache in, 430 
spinal, spastic paraplegia in, 86 
Pain, abdominal, 485 

below diaphragm, twitching of upper 

lip in, 29 
bilateral, of rheumatism of scalp, 

480 
burning, in esophagus, stomach, and 

abdomen in phosphorus poisoning, 

468 
causes of circumscribed abdominal, 
492 

in neighborhood of heart, 481 

in sacral region, 483 

neuralgic, 479 

sciatic, 484 

supra-orbital neuralgic, 479 
colicky, extending to right shoulder 

in acute pancreatitis, 468 
concomitant symptoms of abdomi- 
nal, 23 
crisis of, in tabes, 74 
darting, in urethra, in cystitis, 344 
distribution of, in neuralgia of fifth 

nerve, 479 
expression about eyes in children 
due to, 27 

of face due to, 27 
in abdominal colic, 485 

tumor, 492 
in acute aortitis, 482 
in aneurysm, 271, 482, 490 
in angina pectoris, .481, 482 
in angioneurotic edema, 487 
in appendicitis, 310, 485, 488 
in belly-ache, 20 
in carcinoma of caput coli, 485 
in cardiac disease in children, 22 



INDEX 



529 



Pain in cerebral tumor or abscess, 481 
in chest in aortic aneurysm, 482 
in cholecystitis, 485, 486 
in cholelithiasis, 486 
in coxalgia, 22 
in cystitis, 492 
in dengue, 493 
in diabetes mellitus, 492 
in diarrhea, 22 
in diffuse hepatitis, 486 
in duodenal ulcer, 487 
in dysentery, 334 
in dysmenorrhea, 492 
in dyspepsia, 483 
in enterocolitis, 334 
in enteroptosis, 483 
in fecal impaction, 489 
in fissure of the anus, 492 
in floating kidney, 323, 489 
in gall-stone colic, 321, 485 
in gastralgia, 491 
in gastric cancer and ulcer, 312, 483, 

487 
in head in children, 27 
in hemoglobinuria, 469 
in hemorrhagic infarction, 464 
in hepatic colic, 485 
in hepatitis, 486 
in hip disease, 483, 484 
in indigestion, 485 
in intercostal neuralgia, 481, 482 
in intestinal indigestion, 487 

obstruction, 460, 461, 490 

perforation, 489 
in intussusception, 460, 461 
in jaundice due to gall-stones, 133 
in lead colic, 489 

in locomotor ataxia, 481, 484, 491 
in lumbago, 483 

in lumbar region due to perineph- 
ritic disease, 355 
due to pyelitis, 355 
due to stone in kidney or ureter, 

355 

in malignant growth of femur, 485 

in mediastinal growths, 482, 483 

in meningeal hemorrhage, 430 

in migraine, 480 

in myalgia, 483 

in neuralgia of foot, 492 

of head, 479 

of pelvic viscera, 483 
in neuritis, 479, 484 
in neuromas, 492 
in occipital neuralgia, 480 
in one side of head in migraine, 480 
in pancreatic calculus, 486 
in pancreatitis, 487 
in pelvic growths, 483, 484, 490 
in pericarditis, 482, 483 
in peritonitis, 489 
in pleuritis, 482 
in pseudo-angina pectoris, 481, 482 

^ 34 



Pain in pulmonary diseases in children, 

22 
in pyelitis^ 355, 490, 491 
in rectal disease, 483 
in renal calculus, 485, 490 
colic, 490 
tuberculosis, 490 
in rheumatism of scalp, 480 
in rickets, 483 

in sciatic neuralgia, 483, 484 
in scurvy, 483 
in skin in tabes dorsalis or hysteria, 

190 
in spinal caries, 483 
in strain of sacro-iliac joint, 483 
in syphilitic periostitis of skull, 481 
in typhoid fever, 489 
in uterine disease, 483 
often referred to point distant from 

its source, 479 
sense, 166, 167 
summary of conditions producing 

acute, sudden, 491 
tearing, burning, in hemorrhage into 

membranes of cord, 174 
thoracic, in locomotor ataxia, 482 
throbbing, in inflammation, 478, 492 
varieties of, 478 
Palmus, 63 
Palsy, cerebral, of children, 59 

increased knee-jerk in, 496 
crutch, 61 

infantile, acute, nails in, 50 
ocular, 364 
Pancreas, abscess of, 316 
carcinoma of, 315 
cysts of, 316 

fatty diarrhea due to disease of, 336 
hemorrhagic inflammation of, 316 
inflammation of, 316 

pain in, 487 

symptoms of, 468, 487 

vomiting in, 468 
jaundice in disease of, 135 
Pancreatic calculi in stools, 338 
calculus, pain in, 487 
carcinoma, 315 
cysts, 316 
diabetes, 315 
Pancreatitis, acute hemorrhagic, 316 

vomiting in, 468 
malignant, 316 
Papillitis, 386 

in acute febrile disorders, 387 

in anemia, 387 

in brain tumor, 386, 420, 450 

in cerebral abscess, 387 

in meningitis, 386 

tuberculous, 387 
in rheumatism, 387 
in syphilis, 387 
in toxemia from alcohol, 387 

from lead, 387 



53o 



INDEX 



Papilloma of bladder, hematuria due 

to, 351 
Paresthesia, 186. See also Allochiria. 
brachial, 71 

from exposure to carbolic acid, 187 
in aconite poisoning, 187 
in brain tumor, 187 
in carbolic acid poisoning, 187 
in locomotor ataxia, 187 
in myelitis, 187 
in neurasthenia, 187 
in spinal syphilis, 187 
Paralysis agitans, allochiria in, 187 

festination in, 452 

gait in, 81 

hands in, 59 

Parkinsonian visage in, 30, 452 

speech and voice in, 127 

tremor of hands in, 59, 63 
asthenic, bulbar, 41 

diagnosis between progressive bul- 
bar paralysis and, 41, 42 

speech of, 127 
bilateral facial, 40 
bulbar, acute, 41 

ophthalmoplegia in, 366 

asthenic, 41 

progressive, 41 
cerebral, acute, infantile, causing 
hemiplegia, 122 

deformity of foot in acute, 100 

diagnosis between hysteria and, 87 

gait of infantile, 81 

mirror writing in, 66 

movements of hand in, 66 

spastic paraplegia in, 84 
crossed, 36, 123 
diphtheritic, 41 

dysphagia in, 206, 207 

knee-jerk in, 495 
due to myelitis, 88 

to tumor of brain, 421 
Erb's, 69 

family periodic, 98 
glossolabiopharyngeal, 41 

bilateral atrophy of tongue in, 199 
facial paralysis due to, 41 

biting the tongue in, 198 

cardiac feebleness in, 277 

cough in, 473 

diagnosis of, 127 

dysphagia in, 206 

fibrillary tremor of tongue in, 202 

indistinct speech of mumbling 
character in, 127 

movements of tongue in, 200 

reflexes in, 497 
hysterical, 82 
infantile spinal. See Poliomyelitis, 

anterior. 
Klumpke's, 70 
laryngeal, causes of, 126 
oculofacial, 42 



Paralysis of bladder with retention, due 
to pressure during childbirth, 343 
of insane, progressive, eyes in, 376 
of intra-ocular muscles, 373 
of muscles of jaw, 38 

of leg, 99 
of ocular muscles, 361 

causes of, 365, 366 
of one arm, 66 
of salivary glands, causing dryness 

of mouth, 34 
of tongue, 200 

of vocal cords in aneurysm, 271 
progressive bulbar, 41 
pseudobulbar, tongue in, 200 
recurrent, of oculomotor nerve of one 

side, 40 
reflex, 97 

sometimes found instead of occupa- 
tion spasm, 61 
unilateral facial, 34 
Paralytic chorea, 62 
mydriasis, 376 
myosis, 375 
squint, 362 
Paramyoclonus multiplex, 62 

diagnosis of, 453 
Paramyotonia congenita, 63 
Paraphasia, 128 
Paraplegia, 83 
ataxic, 79, 96 

knee-jerk exaggerated in, 496 
non-spastic, 87, 88, 89 
of rickets, 85 
reflex, 97 
spastic, cerebral, 83, 84 

in arrested development, 84 
hereditary, 86 
spinal lesions causing, 83, 86 
Parasites, anemia due to Ankylosto- 
mum duodenale, 342 
due to tape-worm, 341 
intestinal, Ankylostomum duodenale, 
342 
Ascaris lumbricoides, 342 
Bothriocephalus latus, 340, 341 
Necator americana, 342 
Oxyuris vermicularis, 342 
Tenia cucumerina, 342 
mediocanellata, 340 
solium, 340, 341 
Trichocephalus dispar, 342 
Uncinaria americana, 342 
of lung, Distoma pulmonum, 533 

echinococcus, 533 
of urine, Filaria sanguinis hominis, 352 
Paravertebral triangle of dulness of 

pleural effusion, 251 
Paresis, delusions of grandeur in, 345 
cyanosis in, 140 
diagnosis of coma of, 439 
diplopia a symptom of, 361 
fine intention tremor in, 77 



INDEX 



531 



Paresis, gait of, 77 
hemiplegia in, 123 
Jacksonian epilepsy in, 441, 442 
spasm of tongue in, 202 
tremor of hands in, 65 
vesical symptoms of, 345 
Paretic dementia, bed-sores in, 160 

bilateral atrophy of tongue in, 199 
cyanosis in, 140 
greasy, yellow skin in, 138 
hemiplegia in, 123 
hemorrhages into skin in, 143 
localized sweating in, 162 
optic atrophy in, 388 
perforating ulcer of foot in, 160 
speech in, 127 
tache cerebrale in, 144 
vesical symptoms of, 344 
Parkinson's disease, 30, 64 
Parkinsonian visage, 30, 452 
Paronychia, 50 
Parotitis in pyemic fever, 48 
in typhoid fever, 48 
in typhus fever, 48 
Parrot tongue, 195 
Patellar reflex, 494 
Patient, art of observing, 18 

of questioning, 21 
Pectoriloquy in tuberculosis, 246 

over cavity connected with a bron- 
chial tube, 241 
Pediculi, pigmentation of skin in, 138 
Peliosis rheumatica, 141. See Purpura. 
Pellagra, 150 

Pemphigus, eruption of, 158 
Percussion, direct, 223 

note, coin test in hydropneumotho- 
rax, 252 
cracked-pot sound, 226, 228 
dull, in consolidation of lung in 
pneumonia, 227 
in pulmonary congestion, 249 
edema, 249 
flat, over liver, 225 

pleural effusion, 225, 250 
tympanitic, in lung, due to collapse 
or adhesion of lung, 227 
to consolidation, 227 
to large cavity, 227 
to pneumothorax, 228 
of abdomen, 309 
of heart and great vessels, 228 
of respiratory organs, 225 
of skull, in tuberculous meningitis 

in young children, 427 
resonance, cause of, 224 
trimanual, 325 
Perforating ulcer of foot, 107 
Pericardial adhesion, reduplication of 
heart sounds in, 260 
friction sounds, 269 
Pericarditis, adhesive, 320 
pain in, 482, 483 



Pericarditis, with effusion, diagnosis of, 
from cardiac dilatation, 232 
from hypertrophy, 233 
from mediastinal tumors, 257 
bulging of chest in, 213 
displaced apex beat in, 221 
signs and symptoms of, 231 
Pericardium, adherent, 220 
Perimeter, 380 
Perinephritic abscess, 325 
Periosteal thickening of bones of leg, 

106 
Periostitis of skull, pain in, 481 
Peristaltic waves, 300 
Peritonitis, acute, symptoms of, 309, 
316, 489 
tongue in, 195 
expression of anxiety in, 27, 29 
fever in, 465 
hiccough in, 455 
indicanuria in, 355 
muscular rigidity in, 309 
pain in, 309, 489 
position of body and head in, 20 
pulse in, 280 

small, wiry, 280 
tuberculous, erythema in, 150 
tympanites in, 310 
vomiting in, 465, 470 
Peroneal leg type of progressive mus- 
cular atrophy, 101 
Pes equinus, 101 
Petechia? from drugs, 143 

in acute ulcerative endocarditis, 143 
in cerebrospinal meningitis, 143 
in scurvy, 143 
in septicemia, 143 
in snake-bite, 143 
in typhus fever, 149, 400 
in wasting, 143 
Petit mal. See Epilepsy, minor. 
Phantom tumor of abdomen, 325 
Pharyngitis associated with stomach 
cough, 474 
dysphagia due to, 206, 207 
simple acute, 205 
Phlebitis, fever in, 405 
Phlegmasia alba dolens, 164 

edema in, 164 
Phosphaturia, cloudy urine in, 348 

headache associated with, 419 
Phthiriasis versicolor, skin in, 138 
Phthisis. See also Tuberculosis, 
alar chest of, 212 
cause of night cough in, 473 
character of cough in laryngeal, 472 

of sputum in, 475 
" cog-wheel " breathing an early sign 

of, 23(1 
expansion of chest in, 24(1 
facial expression in, 28 
fibroid, physical signs in, 24b 
flushing of face in, 144 



532 



INDEX 



Phthisis, greasy, yellow skin in, 138 
hands in, 49 

laryngeal, whispering voice in, 125 
night sweats of, 162 
pneumonic, acute, 248 
tongue in advanced, 195 
vomiting in, 469 
Pigeon breast, 213 

Pigmentation of eyelids in pregnancy, 
26 
of skin, 137, 138 
Piles. See Hemorrhoids. 
Plantar reflex, 497 

Pleural effusion. See Effusion, pleural. 
Pleurisy, acute, chest expansion in, 
218 
friction sound in, 239, 249 
pain in, 22, 482 
symptoms and signs of, 249 
tenderness over rib in, 189 
hemorrhagic, 253 
interlobular, physical signs of, 252 
with effusion, 249 
apex beat in, 222 
Baccelli's sign above, 241 
bronchial breathing due to com- 
pression in, 236 
bulging of chest in, 213, 250 
changes in level of effusion in, 

249 
chest expansion in, 218 
convulsions during irrigation of 

pleura in, 450 
cough during aspiration of fluid 
in, 473 
on change of position in, 473 
cracked-pot sound in, 226, 228 
distant breath sounds over effu- 
sion in, 251 
edema over ribs in purulent, 165 
egophony above effusion in, 242, 

. 2 5 J 
Litten's sign of, 219 
method of testing for cause of, 

2 5 x 

of left side, obliteration of 

Traube's semilunar space 

in, 250 

spleen displaced downward 

in, 324 > 

of right side, liver pushed down in, 

3i8 
position in, 20 
pulsating, 223 
vSkodaic resonance above effusion 

in, 227, 250 
symptoms and signs of, 249-251 
vocal freaitus in, 221 
reasonance in, 241 
Pleuritis. See Pleurisy. 
Plumbic gout, 105 

Pneumococcus as a cause of empyema, 
252 



Pneumonia, acute catarrhal, difficulty 
of diagnosis between pulmo- 
nary tuberculosis and, 244, 

* 245 - 
fever m, 413 

physical signs of, 245 
puerile breathing in, 236 
symptoms and signs of, 242, 243 
croupous, casts of finer bronchial 
tubes sometimes found in spu- 
tum of, 477 
blood pressure in, 292 
fever in, 412 
bronchial breathing in, 242, 243 
bubbling rales in resolution in, 238 
Cheyne-Stokes respiration in, 218 
chill in, 390, 412 
chronic Charcot-Leyden crystals in 

sputum of, 477 
cracked-pot sound in, 228 
crepitant rale an early sign of, 238 
crisis in, 243, 412 
crying in children with, 22 
Curschmann's spirals in sputum of, 

477 
delirium in, 243 
diagnosis and symptoms of, 242, 243 

between mediastinal growths and, 

257 
pneumonic phthisis and, 243 
dilatation of pupil in, 376 
expansion of chest in, 219 
expression of anxiety in, 27 
face of, 29 
feeble heart in, 243 
headache in early stages of, 430 
herpetic blisters about mouth, with 

fever in, 29, 158, 243 
increase in urine in convalescence 
from, 348 

of vocal fremitus in, 221 
resonance in, 241 
jaundice in, 137 
necessity for examining axilla and 

septum between upper and middle 

lobe of right lung in, 243, 244 
percussion note dull in, 227, 243 
prune-juice or purulent sputum in, 

243. 474 
pseudocrisis in, 243, 412 
rale redux in, 243 
rapidity of respiration in, 216 
rusty, sticky sputum in, 243, 474, 475 
secondary diphtheritic dysentery due 

to, 335 
subnormal temperature following 

crisis of, 413, 415 
sweat at crisis in, 161 
vocal reasonance in, 241 
wavy breathing of, 218 
Pneumonic phthisis, 243 
Pneumothorax, 253 

amphoric breathing in, 237 



INDEX 



533 



Pneumothorax, bulging of chest walls 
in, 213, 253 
cracked-pot sound in, 226, 228 
decrease of vocal fremitus in, 221 
in pleural effusion, 251 
physical signs of, 253 
tympanic note in, 226, 227 
Poisoning, acute, alcohol, 65, 433 

anesthesia in toxic peripheral neu- 
ritis, caused by arsenic, lead, alco- 
hol, and mercury, 181 
appearance of tongue in acid or 

alkali, 196 
Argyll-Robertson pupil in bisulphide 

of carbon, 374 
arsenical, gait in, 75 
atrophy of tongue in chronic lead, 

199 
auto-intoxication, 418 
blue line on gums in lead, 75, 203 
brachial monoplegia in lead, 70 
cannabis indica, diagnosis of, 434 
chloral, symptoms of, 419, 435 
chronic lead, paralysis in, 61 
constipation in, 330 

gait in, 75 
silver, 137, 139 
constipation in phosphorus, 329 
contraction of pupil in opium, 434 
diplopia in ptomain, spigelia, co- 
nium, belladonna, gelsemium, 361 
edema in arsenic, 164 
fever in septic, 407 
greenish urine in salicylic acid, 354 
hemoglobinuria in mushroom, coal- 
tar, potassium chlorate, glycerin, 
352 
hyperesthesia in lead and arsenic, 

189 
inflammation of Steno's duct in sul- 
phuric acid, 203 
jaundice in phosphorus, 135 

in any poisoning causing exces- 
sive hemolysis, 136 
joint affections in chronic lead, 105 
mercurial tremors in, 63 
myosis in chronic tobacco, 375 
neuralgia of head in lead and arsenic, 

479 

obstinate constipation in chronic 

lead, 330 
ocular paralysis in ptomain, alcohol, 

sulphuric acid, nicotine, lead, and 

carbonic acid, 368 
papillitis in alcohol and lead, 386 
paresthesia in aconite and carbolic 

acid, 187 
phosphorus, constipation in, 329 

stools in, 468 

vomit in, 468 
pin-point pupil in opium, 360 
pruritus in lead and opium, 190 
ptosis in gelsemium and conium, 40 



Poisoning, skin in malarial, 138 

slowness of breathing in opium, 
chloral, aconite, chloroform, anti- 
mony, 217 
tremors of hand in chronic alcohol, 

lead, and mercurial, 63 
urine in santonin and carbolic acid, 

35.4. 
vomiting in antimonial, phosphorus, 

and arsenical, 466 
wrist-drop in lead, 61, 65 
Poliomyelitis, acute, anterior, facial 
paralysis with monoplegia in, 36 
in infancy, hand in, 58 
ophthalmoplegia in, 366 
claw-hand in, 58 
convulsions, headache, and muscular 

twitching in, 95 
crural monoplegia, 101 
diagnosis between acute central my- 
elitis and, 88 
paralysis of leg in, and acute 

cerebral paralysis, 89 
progressive muscular atrophy 
and, 1 01 
fever in, 95, 99 
foot-drop in, 99 
gait in acute, 80 
lateral wrist-drop in, 61 
loss of knee-jerk in, 495 

of power in several muscles of 
limb later in disease in, 95 
paraplegia in, 95, 101 
"Punchinello" leg in, 99 
Polyneuritis, differential diagnosis be- 
tween paraplegia in, and Landry's 
paralysis, 96 
Polyuria, 348 

Posthemiplegic chorea, 121 
epilepsy, 442 
tremor, 65 
Pot-belly, 300 
Pott's disease, 87 

spastic paraplegia in, 87 
Pregnancy, caries of teeth in, 203 
chloasma of, 138 
discomfort due to, 21 
hemorrhagic retinitis in, 388 
pigmentation of eyelids during, 26 
prognosis of acute diffuse nephritis 

in, 356 
vomiting in, 458 
Presystolic mitral murmur, 265 
Prevost's symptom, 471 
Proctitis, symptoms of, 334, 335 
Progressive bulbar paralysis, bilateral 
facial paralysis in. 41 
muscular atrophy, spastic mono- 
plegia in. 100 
Prostate, enlarged, cause, of interfer- 
ence with passage of urine, 347 
Prune-juice sputum in pneumonia , J43. 
474 ' 



534 



INDEX 



Prurigo, pigmentation of skin in, 139 
Pruritus about anus from opium, 190 
in chronic lead poisoning, 190 
in contracted kidney, 190 
in diabetes, 190, 357 
in gout, 190 
in jaundice, 136, 190 
in piles, 190 
Pseudo-angina pectoris, pain in, 481, 

482 
Pseudobulbar paralysis, diagnosis of, 

41, 127, 200 
Pseudocrisis in pneumonia, 412 
Pseudomembranous dysentery, 335 
Pseudomeningitis, convulsions in chil- 
dren in, 450 
Pseudomuscular hypertrophy, gait in, 

80 
Pseudoptosis caused by paralysis of 
the unstriped fibers of Miiller, 38, 39 
Pseudotabes, 75 

gait in, 75 
Pseudotetanus, Escherich's, 451 
Psilosis, 197 
Psoriasis, nails in, 50 
Ptosis, alternate, in so-called nervous 
syphilis, 39 
associated with internal squint, 38 
caused by affection of the sympa- 
thetic, 38 
by cerebral hemorrhage, 38 
by disease of the corpora quadri- 

gemina, 39 
by lesion of oculomotor nerve or 
nucleus, 38 
in angular gyrus, 38 
by nervous syphilis, 39 
by reflex irritation, 40 
complicating tetanus, 40 
concomitant symptoms of, if oculo- 
motor nerve is destroyed, 38 
congenital, 38, 40 
in feeble, overworked women, 40 
in hysteria, 40 

in idiopathic muscular atrophy, 40 
in locomotor ataxia, 40, 361 
in meningitis, 460 
in oculofacial paralysis, 42 
in recurrent paralysis of oculomotor 

nerve on one side, 40 
in tuberculous or syphilitic changes 

at base of brain, 40 
transient, in poisoning by gelsemium 

or conium, 40 
unilateral, 369 

with hemiplegia of face and limbs on 
opposite sides of the body, 40 
Puerile breathing, 236 
Puerperal eclampsia, diagnosis of con- 
vulsions in, 448 
melancholia, lingual spasm in, 202 
Pulmonary abscess, 248 
sputum in, 475 



Pulmonary congestion, 249 
consolidation, position in, 21 
disease in children, pain in, 22 
edema, 249 
gangrene, 249 
breath in, 19 
position in, 21 
vomiting in, 469 
infarction, hemoptysis in, 475 
osteo-arthropathy, feet in, 101 
nails in, 50 

spade-like hands in, 55 
resonance, 225 
stenosis, 268 

valvular murmurs, congenital, 268 
diagnosis of, rules for, 268 
Pulsating pleurisy, 223 
Pulsation, epigastric, 220, 315 
in anurysm, 271 

of retinal arteries in aortic regurgi- 
tation, 267 
on chest wall, 219 
Pulse, bloodvessels and, 278 
causes of rapid, 280 

of slow, 280 
Corrigan, 267, 279 
dicrotic, 281 

disorderly rhythm of, 283 
drop beat, 281 
examination of, 278 
extra systoles, 281 

feeble, rapid, and running, in rup- 
tured compensation of heart mus- 
cles, and in cholera morbus, 331 
force of, 280 
hard and tense, in acute diffuse 

nephritis, 290 
high tension, in acute fevers, 280, 290 
in arteriocapillary fibrosis, 290 
in chronic interstitial nephritis, 

290 
in CO2 poisoning, 290 
in eclampsia, 290 
in labor, 290 
in lead colic, 290 
in pneumonia, 290 
in renal colic, 290 
significance of, 291 
in acute alcohol poisoning, 433, 434 

peritonitis, 280 
in aortic obstruction, 280 

regurgitation, 280 
in chloral poisoning, 435 
in opium poisoning, 434 
in uremic coma, 435 
low tension, in Addison's disease, 294 
in exhausting diseases, 292 
in exophthalmic goitre, 294 
in late stages of acute disease, 295 
in mitral stenosis, 279 
in neurasthenia, 294 
in ruptured compensation, 279 
method of counting, 279 



INDEX 



535 



Pulse, method of production of, 279 
normal limits of, 279 
pulsus alterans, 281 

irregularis perpetuus, 283 
paradoxus, 280 
rapid and weak, in intestinal obstruc- 
tion, 462 
due to stimulation of heart, 280 
slow in cerebral tumor, 422, 459 

of digitalis, 280 
trip-hammer, 267, 279 
volume, 279 
water-hammer, 267, 279 
wave, normal, 279 
Pulsus alterans, 281 

irregularis perpetuus, 283 
paradoxus, 280 
"Punchinello" leg, 99 
Pupil, Argyll-Robertson, 374 
in diabetes mellitus, 74 
in locomotor ataxia, 74 
contracted, 360, 375 
in aortic aneurysm, 271 
from central nervous disease, 360 
from cerebral inflammation, 360 

tumor, 375 
from chronic tobacco poisoning, 

375 
from corneal inflammation, caus- 
ing photophobia, 360 
from locomotor ataxia, 375 
from meningitis, 360, 375 
paretic dementia, 375 
in transverse myelitis, 90 
contraction and dilatation of, with 

Cheyne-Stokes breathing, 377 
dilated, 360 

from blindness, 360 

from fright, 360 

from glaucoma, 360, 376 

from hysteria, 360 

from intracranial pressure causing 

coma, 360 
from irritation of cervical sympa- 
thetic, 375 
of upper part of spinal cord, 

375 . 
from mydriatic, 360 
from paralysis of centre of third 

nerve, 376 
in acute croupous pneumonia, 376 

mania, 376 
in anemia of convalescence, 376 
in aortic aneurysm, 271 
in spinal meningitis, 376 
in tabes dorsalis, 376 
in tumors of spinal cord, 376 

hippus, 376 

Hutchinson's, in cerebral hemor- 
rhage, 120 

immobile, 360, 375 

normal, 374 

pin-point, in opium poisoning, 360 



Pupil, reaction of, abnormal, 374 
to accommodation, 374 
to light, 374 
testing of, 373 
transitory, unequal dilatation of, in 

tuberculosis, 377 
Wernicke's sign of hemiopic inaction 
of, 376, 422 
Purpura hemorrhagica, 142 
hematemesis in, 467 
hematuria in, 352 
hemoptysis in severe, 475 
Henoch's disease in, 143 
in rheumatism, 141, 142 
joint involvement with fever in 
414 
Pus in stools, 338 

in urine, 355 
Pustular syphiloderm, 155 
Putrid bronchitis, 254 
Pyelitis caused by Strongylus gigas, 
352 
chills and fever in, 355, 407 
diagnosis of, 355 
fever in, 355, 407 
pain in, 355, 490, 491 
pyuria constant or intermittent in, 

355 

urine acid in, 355 
Pyelonephritis, 325 
Pyelonephrosis, 325 
Pyemia, chill in, 390 

jaundice in, 137, 138 

joint involvement with fever in, 414 

parotitis in, 48 

profuse sweating in, 162 
Pyemic abscess of liver, 320 
Pylephlebitis, vomiting in, 469 
Pyopneumothorax, coin percussion in, 

2 5 2 
Hippocratic succussion in, 242 
metallic tinkling in, 239 
subphrenicus, 323 



Quincke's sign in aortic regurgitation, 
267 



R 



Radiograph in diagnosis of aortic 

aneurysm, 272 
Railroad-bridge tremor, 65 
Rales, 238 

altered by coughing if not crepitant, 
238 

bubbling, 238 

character of, in asthma, 255 

crepitant, 238 

dry, 238 

moist 238 



53b 



INDEX 



Rales redux in pneumonia, 243 

sonorous, 239 
Raynaud's disease, coma in, 438 
gangrene in, 54, 160 
hands in, 50 
hemoglobinuria in, 352 
localized sweating in, 162 
skin in, 139 
symptoms of, 160 
Rectal catarrh, acute, 334, 335 

disease, pain in, 483 
Reflex iridoplegia. See Argyll-Robert- 
son pupil 

contralateral, in meningitis, 427 

paralysis, 97 
Reflexes, ankle clonus, 498 

biceps tendon, 71, 494 

chin- jerk, 494 

cremasteric, 494 

diseases in which decreased, 495 
in which increased, 496 

in transverse myelitis, 88 

knee-jerk, 494 

loss of ocular, in acute alcoholic poi- 
soning, 434 

of skin, 497, 498 

plantar, 498 

scapulohumeral of von Bechterew, 

494 

tendon, 494 
Regurgitation, aortic, 267 
pulse in, 280 
mitral, 262 

failure of compensation in, 263 
pulse in, 280 
tricuspid, 268 
Relapsing fever, fever in 401 
hematemesis, in 467 
hyperesthesia in, 190 
jaundice in, 136 
spirillum of Obermeier in blood 

in, 401 
sweating in, 162 
tongue in, 193 
Remittent fever. See Malaria, remit- 
tent. 
Renal colic, retraction of abdominal ! 
wall in, 300 
calculus, 351 
cancer, 351 

disease, anasarca in, general, 163 
diarrhea in, 332 
headache in, 419 

pufnness under eyes in, 26, 30, 359 
tuberculosis, 351 
Resonance, vocal, 238, 240 
Baccelli's sign, 241 
decreased, causes of, 241 
increased, causes of, 241 
of chest, 224 
Respiration, causes of labored, 217 
of rapid, 216 
of slow, 217 



Respiration, Cheyne— Stokes, 217 
counting, 216 
in children, 24 
in chloral poisoning, 435 
in coma of apoplexy, 437 
in diabetic coma, 436 
in healthy child, 24 
in uremic coma, 435 
inspiration, prolonged, in spasmodic 

croup, 218 
prolonged expiration in asthma and 

emphysema, 217 
ratio of pulse to, 216 
rhythm of, 217 
stertorous, 434 
wavy, in pneumonia, 218 
Retention cj^sts of pancreas, 316 
of urine in locomotor ataxia, 344 

in myelitis, 343 

in overdistention, 345 

in pressure during childbirth, 345 
Retina, edema of, in arterial disease, 

389 

hemorrhages into, 389 
after suffocation, 389 
in cardiac hypertrophy, 389 
in diabetes, 389 
in gout, 389 
in hemophilia, 389 
in malarial fever, 389 
in septicemia, 389 
in ulcerative endocarditis, 389 
Retinitis, 388 
albuminuric, 388 
hemorrhagic, 388 
in diabetes, 389 
in syphilis, 389 
Retrobulbar neuritis, 387 
Retro-esophageal abscess, 206 
Rheumatic form of gonorrheal arthri- 
tis, 102 
Rheumatism, acute articular, con- 
vulsions in, 414 
cyanosis in, 414 
erythema in, 141 
fever in, 414 
hands in, 53 
headache in, 419 
in knee or ankle, 103 
joint affections in, 414 
papillitis in, 386 
purpura in, 141, 142 
spontaneous dislocation of the 

hip following, 106 
subcutaneous fibrous nodules, 

141 
sweating of, 162 
tongue in, 193 
urticaria in, 145 

with hyperpyrexia, delirium in, 
414 
chronic, hand in, 52 
limping gait in, 73 



INDEX 



537 



Rheumatism, gonorrheal, 102 

of scalp, symptoms of, 480 
Rheumatoid arthritis. See Arthritis 

deformans. 
Rhonchi, 238 

Rhythm, cardiac, disordered, 281, 283 
Ribs, systolic retraction of, in adherent 

pericardium, 220 
Rickets, beaded ribs of, 213, 215 

carpopedal spasm in, 60 

craniotabes in, 46 

deficient bony development in, 46 

early decay of teeth in, 203 

excessive sweating of head in, 47 

facial expression in, 28 

gait in, 80, 83 

Harrison's grooves in, 213 

head in, 28, 46 

hyperesthesia in, 189 

laryngeal spasm in, 256 

nodding spasm in, 44 

open fontanelle in, 46 

pigeon breast in, 213 

pseudoparaplegia in, 97 

spastic paraplegia in, 85 

subperiosteal hematoma in, 105 

sweating of head in, 162 

tenderness of skin in, 189 
Rigidity, intestinal, 325 
Risus sardonicus in epilepsy, 440 

in tetanus or strychnine poisoning, 
26, 43 
Romberg's symptoms, 74, 95 
Rontgen rays in diagnosis of stricture 
of esophagus, 206 
of tuberculosis, 248 
Rose rash, 146. See Erythema and 

Roseola. 
Rotheln, appearance of rash in, 152 

differentiation of, from scarlet fever, 

f I52 - 
fever m, 402 

symptoms of, 152 

Rubella, 152. See Rotheln. 

Rubeola, 153 

Rupia, 148 



St. Vitus' dance. See Chorea. 
Salaam convulsions, 453 
Salivary calculus, 203 
Saltatoric spasm, 453 
Sand, intestinal, 338 
Sarcinse ventriculi in vomitus from 
chronic gastric catarrh, 457 
from dilatation, 457 
from gastric cancer, 457 
from ulcer, 457 
Sarcoma, enlargement of liver in, 318 
melanotic, black urine in, 348 
purpura in multiple, 143 
Scalp, rheumatism of, pain in, 480 



"Scaphoid" belly, 300 
Scapulohumeral reflex of von Bech- 
terew, 494 
in neurasthenia, 494 
Scarlet fever, arthritis in, 104 

Cheyne-Stokes respiration in, 218 

chill in, 390 

collar of brawn in, 402 

date of eruption in, 154 

enlargement of spleen in, 326 

erythema in, 146 

fever in, 401 

gangrene of lower extremities 

after, 107 
hematuria in, 349 
lysis in fever of, 401 
otitis in, 402 

pleurisy with effusion complicat- 
ing, 253 
prognosis from fever, 402 
rose rash in, 146 
sore throat in, 205 
splenic enlargement in, 326 
spontaneous dislocation of hip fol- 
lowing, 106 
strawberry tongue in, 194 
synovitis in, 54 
Schonlein's disease, joint involvement 
in, 105 
symptoms of, 143 
ulcer of buccal mucous membrane 

in, 203 
ulcerations of tongue in, 197 
Sciatica. See Neuritis, sciatic. 
Sciopedy, 102 
Sclerodactyle, nails in, 50 
Scleroderma of tongue, 199 

skin in, 33 
Sclerosis, amyotrophic lateral, 58 
alterations of hands in, 58 
ankle clonus in, 498 
Argyll-Robertson pupil in, 374 
character of speech in, 127 
knee-jerk increased in, 496 
spastic paraplegia in, 85 
disseminated, 187 
ankle clonus in, 497 
coma in, 439 
convulsions in, 450 
differential diagnosis of, 78, 374 
expression of face in, 31 
gait in, 78 

hemianesthesia in, 172 
hemiplegia resulting from. 122 
hippus in, 376 
knee-jerk increased in, 496 
nystagmus in, 373 
optic atrophy in, 388 
paralvsis of ocular muscles in, 
366 
of tongue in, 201 
slow, scanning speech in, 78, 127 
spasm of tongue in, 202 



538 



INDEX 



Sclerosis, disseminated, symptoms of, 65 
tremor of hands in, 64 

of head in, 64 
vertigo in, 432 
general arterial accentuation of 

heart sounds in, 259 
lateral, absence of vesical symptoms 

L in, 344 

ankle clonus in, 497 

1 gait in, 80 

^ increased reflexes in, 85 

> primary, knee-jerk in, 496 

r spastic paraplegia in, 86 

multiple cerebrospinal, 85 
Scorbutus. See Scurvy. 
Scotoma, 387 
Scrofulosis, abdomen in, 300 

dactylitis in, 50 

tongue in, 194 
Scurvy, dropsy in, 164 

ecchymosis under the eyes in, 26 

hematemesis in, 467 

hematuria in, 352 

loosening of teeth in, 203 

pain in back in, 483 

petechiae in, 143 

pseudoparalysis in, in infancy, 95 

skin in, 189 

sponginess of gums in, 203 
Seal-fin hands in arthritic deformans 

and gout, 52 
Senile chorea, 62, 452 

gangrene of foot, 107 
Senility, tremor of hands in, 63 
Septicemia, blood in, 278 

Cheyne-Stokes respiration in, 218 

diarrhea in, 336 

fever in, 407, 411 

great variations in temperature in, 
411 

jaundice in, 135 

petechias in, 143 

retinal hemorrhages in, 389 

rose rash in, 147, 148 
Shiga's bacillus, epidemic dysentery 

due to, 335 
Sibilant rales, 238 
Sigmoiditis, abdominal tenderness in, 

315 

Singultus, 455 

causes of, 455 
Sinus, cavernous, thrombosis of, 428 
lateral, thrombosis of, 428 
superior longitudinal, thrombosis of, 
427 
Skin, anesthesia of, 170 
cadaveric, in pyemia, 138 
cold and moist, with high rectal 
temperature, in sunstroke, 414 
and wet, a bad symptom in fever, 

393 

color of, in health and disease, 131 
cyanosis of, 140 



Skin, cyanosis of, due to laryngeal 
obstruction, 140 

from drugs, 140 

in cardiac disease, 141 

in newborn, 140 

in paretic dementia, 140 
dropsy and swelling of, 163 
dry and hot, in fever, 393 
edema of, 145 

eruptions of, in disease, 141. 
excess of dryness of, 162 
gangrene of, 160 
glossiness of, 159 
greasy yellow, in phthisis and chronic 

liver disease, 138 
greenish yellow, in chlorosis, 138 
harsh, and dry, in acute diffuse 
nephritis, 356 
in cholera, 162 
in diabetes, 162 
hemorrhages into, 143 
hyperesthesia of, 188 
in acute alcohol poisoning, 433, 434 
in Addison's disease, 139 
in angioneurotic edema, 145 
in argyria, 137, 139 
in carcinoma of internal organs, 138, 

139 

in chloasma of pregnancy, 138 

in chromophytosis, 138 

in edema neonatorum, 166 

in elephantiasis, 165 

in influenza, 190 

in jaundice, 131, 132 

in kidney disease, 140 

in ochronosis, 138 

in opium poisoning, 190 

in profound anemia, 190 

in scleroderma, 165 

in tuberculosis, 138 

increased sensibility of, due to ergot, 

190 
leukoderma, in true goitre, 139 
muddy yellow, in chronic malaria 

and prolonged suppuration, 138 
pain of, 190 
pallor of, 139 

in chlorosis, 139 

in myxedema, 140 

in nephritis, 140 

in Raynaud's disease, 139 

in vitiligo, 139 
parchment-like, in syphilis, 26 
pigmentation of, 138 

by the prolonged use of arsenic, 

139 

due to scratching, 138 
paresthesia of, 187 
pigmentation of, due to pediculi, 138 

in exophthalmic goitre, 139 

in _ prurigo, 139 
pruritus of, 190 
redness of, 144 



INDEX 



539 



Skin, scars of, 161 
sensation of, 166 
sweating of, 161 
table of reflexes of, 498 
tache cerebrale, 144 

meningeale, 144 
tactile sensibility of, 167 
tenderness of, in disease of internal 
organs, 190 

in rickets, 189 
thermal sensibility of, 167 
waxy, in cretinism, 31 
yellow, in xanthoma, 141 

and greasy, in paretic dementia, 
138 
Skodaic resonance, 227 
Smallpox, appearance of, eruption in, 

146, 154, 403 
date of eruption in, 154, 155 
fever in, 403 
grisolle sign of, 147 
headache in early stage of, 430 
pain in back in onset of, 493 
Smokers' patch on tongue, 198 
Snake-bite, purpuric eruptions follow- 
ing, 143 
Sonorous rales, 238 
Spasm, blepharofacial, 43 
facial, Abadie's sign in, 43 

in blepharofacial spasm, 43 

in chorea, 42 

in convulsive tic, 42 

in epilepsy, 42, 440 

in hysteria, 44, 447 

in meningitis, 42, 43 

in tetanus, 42, 43 
habit, 42, 62 

hysterical, of esophagus, 207 
laryngeal, 256 

nodding, 44. See Nodding spasm. 
Spasms, 451 
carpopedal, 60 

in adults, due to locomotor ataxia, 
256 

due to mediastinal growths, 256 
in children, due to croup, 256 

due to digestive disturbances, 256 

due to laryngeal catarrh, 256 

due to rickets, 256 
in chorea insaniens, 452 

minor, 451 
in electric chorea, 453 
in Huntingdon's chorea, 452 
in lesion of middle peduncle of cere- 
bellum, 454 
in paramyoclonus multiplex, 453 
in Thomsen's disease, 454 
in true chorea, 452 
laryngeal, in adults, 256 
of fingers due to occupation, 61 
of tongue, 203 
saltatoric, 453 
varieties of, 451 



Spastic infantile hemiplegia, 59 
paraplegia, cerebral, 83 
hereditary, 86 
spinal. 85 
rigidity of arms, 60 
Speech, 125. See also Voice, 
defects of, 127 
agraphia, 128 
alexia, 128 
aphasia, 127 

conduction, 128 
aphemia, 128 
apraxia, 128 
paraphasia, 128 
. tests for, 129 
word blindness, 128 

deafness, 128 
feeble, hesitating, in pneumonia of 
pulmonary edema, 126 
halting, hesitating, in paretic de- 
mentia, 127 
incoherent, in chorea in children, 127 

in delirium, 127 
indistinct, mumbling, 126, 127 
nasal, in adenoid vegetation, 126 
nervous, mechanism of, 128 
scanning, in multiple sclerosis, 79 
shrill, piping, 127 
slow, scanning, in disseminated 
sclerosis, 127 
in Friedreich's ataxia, 127 
tests for defects of, 129 
whispering, causes of, 125 
Sphygmocardiograph, Jacquet's, 284 
Sphygmograph, 282 
Sphygmomanometer, 287, 288 
Mercer, 296 
Nicholson pocket, 296 
Tycos, 297 
Spinal cord, rise in temperature due to 
injuries of, 414 
hemorrhage into, 96 
knee-jerk in injuries of, 495, 496 
lesions causing paraplegia, 83 
localization of functions of seg- 
ments of, 90, 93 
location of lesion of, in anesthesia, 

92, 176 
tumor of, paraplegia in, 95 
irritation, dilatation of pupil in, 375 
Spine, caries of, symptoms of, 483 
Spirillum of Obermeier in blood in 

relapsing fever, 401 
Spirituelle face, 28 

Spleen, causes of enlargement of, 326 
of extension downward, of, 327 
enlarged, in amyloid disease of kid- 
ney, 326 
in Banti's disease, 326 
in cardiac failure, 32b 
in hepatic cirrhosis, 326 
in leukemia, 326 
in leukocythemia, 3 20 



540 



INDEX 



Spleen, enlarged, in malarial fever, 326 
in scarlet fever, 326 
in syphilis, 326 
in typhoid fever, 326 
in Weil's disease, 408 
floating, 327 
Splenic anemia, 326 

fever. See Anthrax. 
Spontaneous dislocation of the hip 

after infectious diseases, 106 
Spots of Valleix, 481 
Spotted fever. See Cerebrospinal men- 
ingitis. 
Sprue, 197 

Sputum, anchovy sauce, 475 
blood-streaked, 475 
bloody, 475 

brick-dust, in hepatic abscess, 475 
brownish, in gangrene of lungs, 249, 

475. 476 
casts of bronchioles m, 477 
Charcot-Leyden crystals in asth- 
matic, 477 
copious and purulent, 249 
Curschmann's spirals in, 476, 477 
Dittrich's plugs in, 254 
frothy, 249, 476 
in asthmatic attacks, 476 
in chronic bronchitis, 254 
in pulmonary gangrene, 249, 475, 476 
liquid and watery, 475 
prune-juice, 243, 474 
purulent, causes of, 475, 476 
rusty and sticky, 474, 475 
semiliquid, 475 
thick and yellowish, 474 
Squint, diagnosis between concomitant 
and paralytic, 362 
of conditions producing, 365 
external and internal, due to tumor 
at base of brain, 421 
causes of, 366, 367, 368 
in hysteria, 372 
in meningitis, 460 
in ocular palsy, 38, 364 
internal, causes of, 367 
significance of external, 368 
Station, in 

in locomotor ataxia, 1 1 1 
Status epilepticus, 446 
Stellwag's symptom, 350 
Stenosis, aortic, 266 
pulse in, 280 

reduplication of heart sounds in, 
260 
mitral, 263 

auricular fibrillation in, 265 
heart block in, 265 
pulse in, 280 
pulmonary, 268 
Steppage gait, 75 
Stereognosis, 168 
Stokes- Adams disease, 276 



Stokes-Adams disease, epileptiform 

seizures in, 449 
Stomach, cancer of, 312 

cough due to reflex irritation from, 

471 

dilatation of_, 304 
vomiting in, 467 
x-ray in diagnosis of, 306 

distention of, by gas, 304 

examination of, 305 

hour-glass, 307 

indicanuria in cancer of, 355 

palpation and percussion of, 309 

ulcer of, 312 

vomiting in dilatation of, 457 
Stomatitis, action of child with, toward 
breast, 23 

buccal mucous membrane in, 203 

impetiginosa, 199 

malignant ulcerative, 203 

offensive odor of breath in, 19 

temperature of mouth raised in, 
392 

tongue in ulcerative, 197 
Stone in bladder, 346 

fecal, 338 
Stools. See also Feces. 

bilious, 337 

bloody, 337, 464 

clay- colored, in hepatogenous 
jaundice, 133 
in Weil's disease, 408 

gall stones in, 338 

in cholera, comma bacilli in, 332 
infantum, 331 

in dysentery, 334 

in intussusception in children, 461 

in proctitis, 334 

intestinal parasite in, 338 

mixed with mucus, 337 

oily, in carcinoma of pancreas, 315 

pus in, 338 

ribbon-shaped, in follicular entero- 
_ colitis, 333 

rice-water, in antimonial poisoning, 
332 . 

tarry, in yellow fever, 408 
Strabismus. See Squint. 
Strawberry tongue, 194 
Streptococci a cause of empyema, 252 
Stricture of esophagus, 206. See Eso- 
phageal stricture. 
Strongylus gigas, hematuria due to, 352 
Stupor in typhoid fever, 397, 400 

in ulcerative endocarditis, 399 
St. Vitus's dance, 452 
Subdural hemorrhage, 438 
Subnormal temperature, 415 
Subperiosteal hematoma, 105 
Subsultus tendinum, 51, 65 
Succussion, Hippocratic, 242 

in pleural effusions with pneumo- 
thorax, 252 



INDEX 



541 



Sudamina, 161 

Summer complaint, 331 

Sunstroke, character of fever in, 414 

diagnosis of coma in, 439 

headache of, 430 

skin cold and moist in, 414 
hot and dry in, 414 
Suppurative tonsillitis, symptoms of, 

206 
" Surgical scarlet fever, " 147 
Sweat, bile-stained, in jaundice, 162 
Symmetrical gangrene, 160 
Syncope, diagnosis of 449 
Synovitis, acute, 103 
Syphilis, action of child with, toward 
breast, 23 

alternate ptosis in, 39 

aortitis in, 482 

Argyll-Robertson pupil in cerebral, 

374 
at base of brain, 40 
broadness of bridge of nose in con- 
genital, 28 
cerebral, coma in, 439 

hemiplegia in, 122 
cerebrospinal, multiple, 78 
cutting of teeth in inherited, 203 
diagnosis between cerebrospinal 
syphilis and disseminated scle- 
rosis, 374 

of coma in, 439 

of epilepsy due to, 443 
enlargement of spleen in early, 326 

of tongue in, 197 
eruptions of, 148, 149 
of liver in, 318 

facial expression in child in, 28 
fever in, intermittent, 414 

remittent, 414 

simple, continued, 414 
fingers in dactylitis in, 50 
fissures and chancres of tongue in, 

197 
gummatous swelling and periosteal 

thickening of shins in, 106 
Hutchinson teeth in, 203 
immobility of pupil in, 374 
miscarriage a symptom of, 21 
mucous _ patches about mouth and 

anus in infantile, 28 
nails in, 50 
of intestinal tract, diarrhea due to, 

335 
open fontanelle in, 46 
pain in periostitis of skull in, 481 
papillitis in, 387 
parchment-like skin of, 26 
paresthesia in spinal, 187 
pseudopalsy in, 70 
ptosis in changes at base of brain in, 

purpura in, 143 

purulent acne of forehead in, 155 



Syphilis, retinitis in, 388 

rose rash in, 148, 149 

scars in, 161 

spastic paraplegia in spinal, 86 

symptoms of arteritis due to, 422 

ulceration of tongue in, 196 
Syphilitic arteritis, 422 
paralyses in, 36 

epilepsy, 443 

gumma, 422 

meningitis, 422 

periostitis of skull, pain in, 481 

rupia, 149 

traid, 203 
Syphiloderm, pustular, 155 
Syringomyelia, nails in, 50 

necrosis of terminal phalanges in, 54 

pain and temperature sense in, 176 

partial anesthesia in, 176 

patches of anesthesia in, 176 

symptoms of, 176 

wasting of hands with anesthesia in, 

59 

Systoles, extra-, of heart, 281 
Systolic blood-pressure, 287, 289 



Tabes dorsalis. See Locomotor ataxia. 
Tabetic atrophy of foot, 102 
of optic nerve, 388 
ulcer, 106 
Table of reflexes, '498 
Tache cerebrale, 144 
meningeale, 144 
Tachycardia, 276 
Tactile sensibility of skin, 167 
Talipes equinovarus in Friedreich's 

ataxia, 78 
Tape- worm. See Parasites; Tenia. 
Tarbadillo fever, 401 . 
Taste, decrease of acidity in, of facial 
hemiatrophy, 32 
loss of, in anterior portion of tongue 
in disease of petrous portion of 
temporal bone, 34 
Tenia cucumerina, 342 
mediocanellata, 340, 341 
solium, 340, 341 
Teeth, ages at which different, appear 
in children, 202 
blue line around, in lead poisoning, 

203 
caries of, in diabetes mellitus, 203 

in pregnancy, 203 
decay of, in rickets, 203 

early, in inherited syphilis, 203 
grinding of, in children, 203 
Hutchinson. 203 
loosening of, in salivation, 203 

in scurvy, 203 
staining of, 203 



542 



INDEX 



Temperature. See also Fever, 
in acute alcohol poisoning, 433 
in cholera Asiatica, 331 

infantum, 331 
in diabetic coma, 436 
in injuries to cervical cord, 415 
in intestinal obstruction, 462 
in typhoid fever, 394 
in uremic coma, 435 
subfebrile, mildly febrile, decidedly 

febrile, 390 
subnormal, causes of, 415 
in cretinism, 31 
in heart exhaustion, 415 
in injuries to dorsal portion of 

spinal cord, 415 
in pernicious malaria, 415 
Tendon reflexes, 494 
Tenesmus in bladder trouble, 343 
in cholera infantum, 331 
in dysentery, 334 
in intussusception, 461 
in proctitis, 334 
in stricture of rectum, 333 
Tension, arterial, 286 
low, 292 
normal, 287 

estimation of, 287 
high, temporary, 289 
persistent, 290 
significance of, 291 
asynchronous, of sigmoid valves caus- 
ing reduplication of second sound 
of heart, 260 
Tetanus, convulsions in, 450 
facial spasm in, 42, 43 
head or cephalic, 45 
knee-jerk increased in, 496 
ptosis in, 40 

risus sardonicus in, 26, 43 
Tetany, "accoucheur's hand" in, 60, 

451 

character of convulsions in, 451 
Chvostek's symptom of, 451 
Erb's symptom of, 451 
gastric dilatation in, 60 
laryngismus stridulus in, 451 
thyroid wasting in, 60 
Trousseau's symptom of, 451 
Thermic fever. See Sunstroke. 

sensibility of skin, 166 
Thomsen's disease, diagnosis of, 454 
spasm of hand in, 63 
of tongue in, 202 
Thorax, aneurysm of, diagnosis be- 
tween medicinal growths and, 

257 
localized sweating in, 162 
spongy, venous masses above 
clavicle due to, 219 
inspection of, 208 
Thread-worms, 342 
Thrill, causes of, 223 



Thrill, diffuse and feeble, in cardiac 
dilatation, 273 
in aortic aneurysm, 269 
in carotid arteries, 276 
in hydatid cyst of liver, 320 
in mitral regurgitation in children, 

262 
stenosis, 263 
Thrombosis, cerebral, 59 

brachial monoplegia in, 67 
bulging fontanelle in, 121 
coma in, 438 
edema in, 163, 164 
hemiplegia in, 121 
of lateral sinus, Gerhardt's symp- 
tom of, 429 
of superior longitudinal sinus, 427 
of cavernous sinus, 428 
of coronary artery, 275 
of femoral artery, 106 
of lateral sinus, 428 

localized edema in, 164 
of renal vein causing hematuria, 350 
of umbilical vein in melena neona- 
torum, 467 
of vena* azygos a cause of serous 

pleural effusion, 251 
vomiting in, 459 
Thrush, tongue in, 194 
Thyroid wasting in tetany, 60 
Tic, convulsive, 63 

facial spasm in, 42 
Tinnitus aurium in Meniere's disease, 

456, 469 
Tobacco amblyopia, 387 

heart, 275 
Toe, tender, in sciatica, 484 
Toes, separation of, in ainhum, 108 
Tongue, annulus migrans of, 199 
bilateral atrophy of, 199 
biting of, 198 
chancre of, 197 ■ 

chronic superficial glossitis of, 198 
coating of, unilateral, due to decayed 

teeth or hemiplegia, 195 
dryness or moisture of, 195 
enlargement of, in acromegaly, 200 
epithelioma of, 197 
eruptions of, 198 
examination of, 191 

in children best when crying, 24 
fibrillary tremor of, 202 
fissures of, 196 
geographical, 199 
glossodynia exfoliativa of, 198 
hemiatrophy of, 200 
ichthyosis of, 198 
in acute articular rheumatism, 193 
catarrhal jaundice, 193 
gastric catarrh, 194 
in children, 194 
inflammation of, 199 
in Addison's disease, 196 



INDEX 



543 



Tongue, in advanced disease of exhaust- 
ing nature, 195 

in anemia, 195 

in biliousness, 193 

in cardiac disease, 195 

in cretinism, 31 

in dysentery, 195 

in grave disease of the viscera, 195 

in hemiplegia, 195 

in hepatic abscess, 195 

in mucous disease, worm-eaten, 194 

in persons taking large amounts of 
milk, 194 

in poisoning by acids, 196 
by alkalies, 196 
by cantharides, 196 
by corrosive sublimate, 196 

in pulmonary disease, 195 

in relapsing fever, 193 

in scarlet fever, 194 

in scrofulosis, 194 

in stomatitis impetiginosa, 199 

in syphilis, 196 

in thrush, 194 

in tonsillitis, 192 

in typhoid fever, 192 

in ulcerative stomatitis, 197 

in uremia, 193 

leukokeratosis of, 198 

leukoma of, 198 

lichen planus of, 198 

movements of, 200 

mucous patches of, 197 

mycosis of, 194 

edema of, 199 

paralysis of, 200 

parrot, 195 

patches on, 198 

purple spots on, in Addison's disease 

195 

scleroderma of, 199 

smokers' patch on, 198 

spasm of, 202 

stains of, 195 

strawberry, in scarlet fever, 194 

tremor of, in alcoholism, 202 

in glossolabiopharyngeal paralysis, 

202 
ulceration of, 197 
unilateral atrophy of, in chronic lead 

poisoning, 199 
urticaria of, 198 
wandering rash of, 199 
worm-eaten, in mucous disease, 194 
xanthelasma of, 196 
xeroderma pigmentosum of, 198 
Tonsillitis, breath in, 19 
chronic night cough in, 473 
diagnosis between diphtheria, scarlet 

fever, and, 204 
dysphagia in, 206, 207 
fever in, 204 
odor of breath in, 19 



Tonsillitis, suppurative, 204 
symptoms of, 204 
tongue in, 192 
Tonsils, chronic cough in enlarged lin- 
gual, 473 
night cough in enlarged faucial, 473 
symptoms of chronic enlargement of, 
204 
Torula cerevisiae causing fermentation 

in gastric dilatation, 457 
Toxic amblyopia, 387 
Tracheal tugging in aneurysm, 272 
Transudations into pleural cavities, 251 
Traube's semilunar space obliterated in 

left-sided pleural effusion, 250 
Tremor of hands and arms, 63 

in disseminated sclerosis, 64 , 
in general paresis, 65 
in Graves' disease, 63, 65 
in hysteria, 65 

in mercurial poisoning, 63, 64 
in paralysis agitans, 63 
railroad-bridge type of, 65 
of tongue, 201 
of type Rendu, 65 
posthemiplegic, 65 

sometimes found instead of occupa- 
tion spasm, 61 
Triangle, Fenwick's, 268 
Triangles, cardiac, 229, 230 
Trichiniasis, diagnosis of, 400 

puffy eyelids in, 30, 31 
Trichinosis. See Trichiniasis. 
Trichocephalus dispar, 342 
Tricuspid regurgitation, 268 

stenosis, 268 
Trimanual percussion, 325 
Trip-hammer pulse of aortic regurgita- 
tion, 267, 279 
Tropical abscess of liver, 320 

dysentery, 334 
Trousseau's symptom of tetany, 451 
Tube casts. See Casts. 

of choroid, 426 
Tuberculosis a cause of empyema, 253 
amphoric breathing in, 237, 246 
bronchial breathing and consolida- 
tion in, 236 
bronchitis a cause of death in, 22 
bronchophony in, 246 
bubbling rales in, 238, 246 
Charcot-Leyden crystals in, 477 
Cheyne-Stokes breathing in menin- 
geal, 217 
chill in, 390 

chronic loose morning cough in, 472 
cracked-pot sound in, 206, 20S 
crepitant rales and breaking down of 

lung tissue in, 238 
cyanosis in acute miliary. 412 
dactylitis in, 50 

diagnosis between catarrhal pneu- 
monia and pulmonary, 245, 240 



544 



INDEX 



Tuberculosis, diarrhea of, 334 
expiration prolonged in, 246 
fever in acute miliary, 412 

pulmonary, 411 
frog-belly in, 300 
heavy face in bone disease in, 28 
hectic fever in, 246 
hemoptysis in, 475 
hemorrhagic pleurisy in, 253 
hoarseness in, 125 
hollow-chested build in, 17 
loss of flesh in, 246 
mammary glands enlarged in, 215 
metallic tinkling in, 239 
multiple ulceration of tongue in, 197 
necessity of examining axilla in, 249 
ocular palsy in, 366 
of bladder, hematuria due to, 351 
of kidney, 351, 490 
of mesenteric glands, 315 
of omentum, 315 
pectoriloquy in, 246 
percussion note dull in consolidation 

due to, 227 
pleurisy complicating, 251 
ptosis in changes at base of brain due 

to, 40 
puerile breathing an early sign of, 236 
rapidity of breathing in, 216 
retraction of abdominal wall in, 300 
Rontgen rays in diagnosis of, 248 
scars on neck from suppurating 

glands in, 161 
spirituelle face of children with 

diathesis of, 28 
sputum, Curschmann's spirals in, 

476, 477 
sweating in, 162 
tongue in, 195 
transitory, unequal dilatation of 

pupils in, 376, 377 
vocal fremitus and resonance in- 
creased in, 221, 241, 246 
vomiting in acute miliary, 460 
Wintrich's change of percussion note 

in, 246 
Tuberculous glands, symptoms of, 315 
meningitis, 425 

differential diagnosis of, 425 

headache in, 425 

in children, 425 

Kernig's sign in, 427 

lumbar puncture in, 410, 426 

papillitis in, 387 
pyelitis, 355 < 
Tubular breathing, 235, 236 
Tumor, abdominal, pain in, 491 
at base of brain, symptoms of, 36 
brain, Cheyne- Stokes breathing in, 
217 

contracted pupil in, 375 

hyperesthesia in. 189 

impaired memory in, 459 



Tumor, brain, monoplegia in, 67 

papillitis in, 387, 459 

paresthesia in, 187 

severe headache in, 459 

slow pulse in, 459 

spastic hemiplegia in, 122 

symptoms of, 420 

unilateral anesthesia in. 172 

vertigo in, 432. 459 

vomiting independent of taking 
food in, 459 
of chest, 257 
diagnosis of fatty, in abdominal wall, 

3ii 

in intussusception, 460 

in renal pelvis, symptoms of, 489 

of abdomen, 303, 311, 316 

of bladder, 345 

of cord, bladder symptoms of, 345 

dilatation of pupil in, 376 

girdle sensation in, 188 

of lung, rapid respiration in, 216 

of mediastinum, 256 

of nerves, pain in, 492 

of omentum, 316 

paraplegia in, 97 

phantom, 325 

pontine, anesthesia in, 173 
Tycos sphygmonometer, 297 
Tympanites in flatulent colic, 299, 

in intestinal obstruction, 463 
in peritonitis. 300 
in typhoid fever, 300 399 
Typhoid fever, bacillus of Eberth the 
cause of, 399 
bed-sores in, 160 
bloody stools in, 337, 464 
bradycardia in, 276 • 
carphologia in, 66 
Cheyne- Stokes respiration in, 218 
chill in, 390 
coma in, 436 
delirium in, 29, 399 
diagnosis, 400 

between acute miliary tubercu- 
losis and, 399 
Malta fever and, 400 
relapsing fever and, 401 
remittent fever and, 397, 398 
trichiniasis and, 400 
typhus fever and, 400 
ulcerative endocarditis and, 

399 . 

edema of thigh over deep muscular 
abscess following, 165 

enlargement of spleen in, 326, 399 

eruption in, 149, 397 

face in, 29 

fever in, 394 

gangrene of lower extremities fol- 
lowing, 107 

headache in, 430 



INDEX 



545 



Typhoid fever, hyperesthesia in conva- 
lescence from, 189 

hypertrophic osteoarthritis follow- 
ing, 104 

in children, 408 

increase of urine in convalescence 
from, 348 

lesions of lungs in, 399 

meteorism in, 398 

milk leg after, 106 

moderate bronchitis in, 399 

mushy stool in, 336 

pain in, 489 

phlegmasia alba dolens in, 164 

pleurisy with effusion complicat- 
ing, 252 \ 

recrudescence in, 395 

relapse in, 397 

roseola in, 148, 149,397 

speech in, 126 

splenic enlargement in, 326 

spontaneous dislocation of the hips 
following, 106 

stools in, 397, 399 

stupor in, 397, 399 

subsultus tendinum in, 65 

sweating in, 162 

temperature, 395 

tongue in, 192 

tympanites in, 300, 399 

vomiting in, 465 

Widal's test for, 397 

without fever, 397 
Typhomalarial fever. See Malaria, 

remittent. 
Typhus fever, crisis in, 400 
. eruption in, 149, 400 

exhaustion in, 400 

fever in, 400 

hematemesis in, 467 

headache in, 400 



Ulcer, duodenal, 313 
pain in, 487 
of stomach, hematemesis in, 466 
symptoms of, 312 
vomiting in, 466 
perforating, of foot, 106 
tabetic, of foot, 106 
Ulcers at base of finger nails, 50 

on buccal mucous membrane in 

Schonlein's disease, 203 
on tongue, 197 
perforating, in diabetes, senility, and 

tabes dorsalis, 106 
syphilitic, in intestinal tract causing 
diarrhea, 335 
Umbilical hernia, 326 
Uncinaria americana, 342 
duodenale, 342 



Unconsciousness. See Coma. 
Unilateral anesthesia, 172 

facial paralysis, 34. See Paralysis. 

mydriasis, 376 

ptosis, 369 

reflex iridoplegia, significance of, 

375 

wrist-drop, 61 
Uremia. See also Coma, 
amaurosis in, 383, 459 
Babinski reflex in threatened, 420 
breath in, 19 

Cheyne-Stokes breathing in, 217 
colliquative diarrhea in, 459 
coma in, 436 

in chronic interstitial nephritis, 

357 
convulsions in, 445, 448 
headache in, 419, 420 
hiccough in, 455 
sweating in, 162 
symptoms of, 436 
tongue in, 193 

vomiting in, 436, 455, 456, 458 
Urethra, fever due to passage of sound 
into, 394 . 

incontinence of urine due to insensi- 
tive, 345 . 
interference with passage of urine in 
stricture of, 346 
Urecemia. See Lithemia. 
Uridrosis, 162 
Urine, bile in, 354 

Gmelin's test for, 354 

stained, in hepatogenous jaundice, 

133 

blood in, 348 
color of, blue, 353 

brown, 353 

causes of black, 348 
of changes in, 348 

due to blood, 348 

green, 353, 354 

in diabetes, 353 

in iaundice, 353, 354 

red, 348, 353, 354 

white or milky, 353, 354, 355 

yellow, 353 
collecting of, for testing, 347 
dark, not due to blood, 354 
in acute diffuse nephritis, 356 
in apoplexy, 346 
in cholera morbus, 330 
in chronic interstitial nephritis, 357 
in diabetes mellitus, 357 
in hepatogenous jaundice, 133 
in idiots, 346 
in infectious diseases, 346 
in intestinal obstruction, 463 
in irritation of foreskin or vagina in 

children 346 
in phosphorus poisoning, 468 
in pyelitis, 355 



546 



INDEX 



Urine in seat-worms, 346 

in some cases of insanity, 346 

in uremia, 435 

incontinence of, 345 

indican in, 355 

odor of, causes of alteration of, 348 

pus in, 355 

due to calculus, 355 

in pyelitis, 355 

in tuberculosis of kidneys, 355 

quantity of, causes of alteration in, 347 

retention of, 343 

variations in quantity of, 347 
Urobilin icterus, 136 
Urticaria, 147 

from drugs, 145 

in rheumatism, 145 

of tongue, 198 
Uterine disease, pain in, 483 



V 



Vaccination, eruption of, 154 

roseola following, 146 
Vaccinia, 156 

Valvular heart disease. See Heart. 
Varicella. See Chicken-pox. 
Variole. See Smallpox. 
Vena azygos, thrombosis of, as a cause 

of serous pleural effusion, 251 
Vertigo, 431 

due to drugs, 432 

in anemia, 432 

in aortic obstruction, 267 

in apoplexy, 432 

in brain tumors, 432, 459 

in disseminated sclerosis, 432 

in epilepsy, 432 

in indigestion. 432 

in ingravescent apoplexy, 118 

in Meniere's disease, 432 

in middle-ear disease, 432 

in ocular palsy, 365 

in paretic dementia. 123 

paralyzing, 432 
Vesical crises in locomotor ataxia, 74, 

351 

Vesicular breathing, 235 
Vision, changes in acuity of, 377 

failure of, 377 
Vitiligo, 139 

Vocal fremitus, 220. See Fremitus 
vocal. 

resonance See Resonance, vocal. 
Voice. 125 

hoarseness of, 125 

in aneurysm, 125 

in paralysis agitans, 127 

in typhoid fever, 126 

loss of, or mutism, 125 

nasal, causes of, 126 

whispering, causes of, 125 



Volvulus, 464 
Vomit, 470 

in cerebral disease, 470 
in intestinal obstruction, 470 
in migraine, 470 
in peritonitis 470 
in phosphorus poisoning, 468, 470 
in yellow fever, 408 
of chronic gastric catarrh, 456, 470 
of gastric cancer, 312, 466 
dilatation, 457 
ulcer, 466 
of uremia, 458, 470 

for sarcinae in. 457 
Vomiting, 455 

associated with headache, 456 
bilious, in remittent malarial fever, 

407 
black, in yellow fever, 408 
centric, from chloroform or ether, 455 
coffee-ground, in gastric cancer, 312, 
466, 467 

in locomotor ataxia. 467 

in phosphorus poisoning, 468 
cyclical 467 

decrease of urine by persistent, 348 
due to injuries to the epigastrium, 

467 
in acute gastric catarrh, 456 

gastric miliary tuberculosis, 460 

infectious diseases, 456 
pancreatitis, 468 
yellow atrophy of liver, 469 
in antimony poisoning, 466 
in apoplexy, 456 
in appendicitis, 465 
in brain abscess, 456 

tumor, 420, 456 
in catarrhal or obstructive jaun- 
dice, 469 
in cerebellar tumor, 456 
in cerebral anemia, 459 

embolism, 459 

hemorrhage, 459 

thrombosis, 459 
in cerebrospinal meningitis, 410 
in cholera Asiatica, 456, 465 

in infantum, 331, 465, 466 

morbus, 331, 466 
in chronic gastric catarrh,. 456 
in congenital hypertrophic stenosis 

of pylorus, 464 
in croupous pneumonia, 456 
in diabetes, rarely, 459 
in dilatation of the stomach, 457 
in dysentery, 466 
in early secondary syphilis, 470 
in erysipelas 470 
in exophthalmic goitre, 458 
in gastric cancer, 456, 466 

catarrh, acute, 456 
chronic, 456 
indigestion, 456 



INDEX 



547 



Vomiting in gastric ulcer, 456, 466 

in gastritis, 456 

in hemiplegia due to hematoma of 
dura mater, 122 

in hemoglobinuria, 469 

in hemorrhagic infarction of intes- 
tine, 464 
pressure on brain, 122 

in hepatic abscess, 469 
cirrhosis, 467 
colic, 456 
jaundice, 456 

in hepatitis, 469 

in hysteria, 456, 457 

in influenza, 412 

in ingravescent apoplexy, 118 

in intestinal indigestion, 456 

in intestinal obstruction, 330, 456, 
460, 461, 462 

in intussusception, 460 

in locomotor ataxia following gas- 
tric crisis, 457 

in melena neonatorum, 467 

in Meniere's disease, 456. 469 

in meningitis, 460 

in merycismus, 470 

in migraine, 456 

in nephritic colic, 456 

in neurasthenia, 457 

in neuroses of stomach, 457 

in pellagra, 150 

in peritonitis, 456, 464 

in phosphorus poisoning, 468 

in phthisis, 469 

in poisoning by arsenic and anti- 
mony, 466 

in pregnancy, 458 

in profound cerebral anemia, 459 

in pulmonary gangrene, 469 

in purulent meningitis, 459 

in pylephlebitis, 469 

in renal calculus, 469 

in true gastritis, rare, 456 

in typhoid fever, 465 

in uremia, 436, 455, 456, 458 

in whooping-cough, 469 

in yellow fever, 456, 408, 469 

of blood. See Hematemesis. 

uremic, in chronic parenchymatous 
nephritis, 357 



W 



Wasting of hand, 55 
"Water-hammer pulse" of aortic regur- 
gitation, 267, 279 
Wavy breathing in pneumonia, 218 
Weil's disease, absence of gastrointes- 
tinal symptoms in, 408 

clay-colored stools in, 408 

fever in, 408 

jaundice in, 135, 408 

swelling of liver and spleen in, 408 



Wernicke's pupil, 376, 422 

Westphal's sign, 74 

Whip- worm, 342 

Whispering voice, 125 

White urine, 355 

Whitlow, painless, in Morvan's disease, 

5 8 
Whooping-cough, Cheyne-Stokes respi- 
ration in, 218 

cough in, 471 

hemorrhage of skin in, 143 

ulcer on frenum in, 197 

vomiting in, 469 
Wintrich's change of percussion note in 

tuberculosis, 246 
Word blindness, 128 

deafness, 128 
" Worm-eaten "tongue in mucous dis- 
ease, 194 
Worms, 338 

involuntary passage of urine due to 
seat-, 346 
Wrist-drop, causes of, 61 
Wrist-jerk, marked, in amyotrophic 

lateral sclerosis, 58 
Wry-neck, clonic, or tonic, 44 

congenital or acquired, 44 

diagnosis of, 44 

facial asymmetry in connection with, 
32 



Xanthelasma, 196 
Xanthoma, 141 
Xeroderma pigmentosum, 198 
X-ray in gastric dilatation, 306, 307 
in diagnosis of, 306 



Yellow atrophy of liver, coma in, 436 
hematemesis in, 467 
jaundice in, 135 
symptoms of, 136 
fever, black vomit in, 408 
diagnosis of, 408, 409 

between bilious remittent fever 

and, 409 
between dengue and, 408 
fever in, 408 
hematemesis in, 467 
hemorrhage from mucous mem- 
branes in, 408 
jaundice in, 136, 408 
symptoms of, 469 
tarry stools in, 408 
vomiting in, 469 
spot of the eye, 386 



Zones, hysterogenous, [88 



